Loading [MathJax]/jax/output/SVG/jax.js
Review

Sensitization to cell death induced by soluble Fas ligand and agonistic antibodies with exogenous agents: A review

  • Received: 16 July 2020 Accepted: 18 August 2020 Published: 25 August 2020
  • Specific binding of either soluble Fas ligand extracellular domain (sFasL) or agonistic anti-Fas receptor extracellular-domain monoclonal-antibodies (FasR-mAb) can trigger apoptotic death of emerging harmful cells in the human body. However, the efficient cell-death induction through the action of these executors are often prevented by the resistance mechanisms equipped with the target cells. Hence, strengthening their cell-death inducing activity by sensitization with the help of exogenous agents will contribute to the development of advanced treatment strategies for many serious diseases caused by impaired cell death, including cancers and autoimmune diseases. This review gives an overview focusing on the sensitization of the cell-death induction via either sFasL- or FasR-mAb-primed signal transduction system with exogenous agents. In the beginning section, the structural and functional characteristics of cell-death induction using these soluble agonistic proteins were briefly introduced. In the following sections, the studies on the sensitization of Fas signaling system with the exogenous agents, classified into two groups, were investigated, based on an extensive survey of the relevant literatures. First, the sensitization with non-cytokine agents was described, where the effects of representative low molecular-weight clinical anticancer drugs were highlighted. Then, the potency of exogenous cytokine agents was depicted, while centering on the sensitization with interferon-γ. The survey revealed that the agents examined here were effective for the sensitization against various malignant tumors-derived and other types of cells by upregulating pro-apoptotic molecular machinery and/or downregulating anti-apoptotic factors. However, in the demanding instances, this strategy still remained dysfunctional in completing the target cell-killing process due to resistance mechanisms, such as overexpression of intracellular inhibitory proteins. Finally, it is proposed that the sensitization of cell-death induction with exogenous agents, combined with empowerment regarding the targeting specificity by protein engineering techniques, is a promising approach to potentiate the soluble agonists for translating them into clinical protein pharmaceuticals.

    Citation: Michiro Muraki. Sensitization to cell death induced by soluble Fas ligand and agonistic antibodies with exogenous agents: A review[J]. AIMS Medical Science, 2020, 7(3): 122-203. doi: 10.3934/medsci.2020011

    Related Papers:

    [1] Ming Chen, Menglin Gong, Jimin Zhang, Lale Asik . Comparison of dynamic behavior between continuous- and discrete-time models of intraguild predation. Mathematical Biosciences and Engineering, 2023, 20(7): 12750-12771. doi: 10.3934/mbe.2023569
    [2] Renji Han, Binxiang Dai, Lin Wang . Delay induced spatiotemporal patterns in a diffusive intraguild predation model with Beddington-DeAngelis functional response. Mathematical Biosciences and Engineering, 2018, 15(3): 595-627. doi: 10.3934/mbe.2018027
    [3] Adnan Sami, Amir Ali, Ramsha Shafqat, Nuttapol Pakkaranang, Mati ur Rahmamn . Analysis of food chain mathematical model under fractal fractional Caputo derivative. Mathematical Biosciences and Engineering, 2023, 20(2): 2094-2109. doi: 10.3934/mbe.2023097
    [4] Peter A. Braza . Predator-Prey Dynamics with Disease in the Prey. Mathematical Biosciences and Engineering, 2005, 2(4): 703-717. doi: 10.3934/mbe.2005.2.703
    [5] Jie Hu, Juan Liu, Peter Yuen, Fuzhong Li, Linqiang Deng . Modelling of a seasonally perturbed competitive three species impulsive system. Mathematical Biosciences and Engineering, 2022, 19(3): 3223-3241. doi: 10.3934/mbe.2022149
    [6] Jian Zu, Wendi Wang, Bo Zu . Evolutionary dynamics of prey-predator systems with Holling type II functional response. Mathematical Biosciences and Engineering, 2007, 4(2): 221-237. doi: 10.3934/mbe.2007.4.221
    [7] Moitri Sen, Malay Banerjee, Yasuhiro Takeuchi . Influence of Allee effect in prey populations on the dynamics of two-prey-one-predator model. Mathematical Biosciences and Engineering, 2018, 15(4): 883-904. doi: 10.3934/mbe.2018040
    [8] Yazhi Wu, Guangyao Tang, Changcheng Xiang . Dynamic analysis of a predator-prey state-dependent impulsive model with fear effect in which action threshold depending on the prey density and its changing rate. Mathematical Biosciences and Engineering, 2022, 19(12): 13152-13171. doi: 10.3934/mbe.2022615
    [9] Gianni Gilioli, Sara Pasquali, Fabrizio Ruggeri . Nonlinear functional response parameter estimation in a stochastic predator-prey model. Mathematical Biosciences and Engineering, 2012, 9(1): 75-96. doi: 10.3934/mbe.2012.9.75
    [10] Saheb Pal, Nikhil Pal, Sudip Samanta, Joydev Chattopadhyay . Fear effect in prey and hunting cooperation among predators in a Leslie-Gower model. Mathematical Biosciences and Engineering, 2019, 16(5): 5146-5179. doi: 10.3934/mbe.2019258
  • Specific binding of either soluble Fas ligand extracellular domain (sFasL) or agonistic anti-Fas receptor extracellular-domain monoclonal-antibodies (FasR-mAb) can trigger apoptotic death of emerging harmful cells in the human body. However, the efficient cell-death induction through the action of these executors are often prevented by the resistance mechanisms equipped with the target cells. Hence, strengthening their cell-death inducing activity by sensitization with the help of exogenous agents will contribute to the development of advanced treatment strategies for many serious diseases caused by impaired cell death, including cancers and autoimmune diseases. This review gives an overview focusing on the sensitization of the cell-death induction via either sFasL- or FasR-mAb-primed signal transduction system with exogenous agents. In the beginning section, the structural and functional characteristics of cell-death induction using these soluble agonistic proteins were briefly introduced. In the following sections, the studies on the sensitization of Fas signaling system with the exogenous agents, classified into two groups, were investigated, based on an extensive survey of the relevant literatures. First, the sensitization with non-cytokine agents was described, where the effects of representative low molecular-weight clinical anticancer drugs were highlighted. Then, the potency of exogenous cytokine agents was depicted, while centering on the sensitization with interferon-γ. The survey revealed that the agents examined here were effective for the sensitization against various malignant tumors-derived and other types of cells by upregulating pro-apoptotic molecular machinery and/or downregulating anti-apoptotic factors. However, in the demanding instances, this strategy still remained dysfunctional in completing the target cell-killing process due to resistance mechanisms, such as overexpression of intracellular inhibitory proteins. Finally, it is proposed that the sensitization of cell-death induction with exogenous agents, combined with empowerment regarding the targeting specificity by protein engineering techniques, is a promising approach to potentiate the soluble agonists for translating them into clinical protein pharmaceuticals.


    Bearing is an important component of rotating machinery and has been widely used in various fields such as automation and medical treatment. Due to the harsh and complex working environment, it has become one of the most vulnerable parts of mechanical equipment. Its running state directly affects the safety, reliability, and service life of the whole mechanical system ADDIN EN.CITE.DATA [1]. Therefore, it is extremely important to conduct fault diagnosis research on bearings. Bearing fault diagnosis is very complicated, especially since its early fault signal is extremely weak, which is easy to be submerged in the noise signal of other components and cannot be detected ADDIN EN.CITE.DATA [2]. However, the above-mentioned traditional vibration analysis method and current analysis method mainly classify the bearing faults at high speed, and it is difficult to accurately classify the vibration signals buried in noise and the current signals in the low-speed bearing faults. Compared with vibration analysis ADDIN EN.CITE.DATA [3,4,5] and current signal analysis ADDIN EN.CITE.DATA [6], AE signal has the following advantages: a) It is not affected by mechanical background noise; b) It is more sensitive to early and low-speed bearing faults; c) It is sensitive to the location of the fault; d) It can provide good trend parameters; e) It has the characteristics of high frequency and obvious frequency ADDIN EN.CITE.DATA [7]. Due to the above advantages, bearing fault diagnosis based on AE signals has been widely used, and some research results have been obtained. However, AE technology has the disadvantages of a large amount of time-domain data and difficulty in storage and processing. At the same time, high-frequency AE signals are accompanied by high sampling rates, and the combination of high sampling rates and massive data will bring greater challenges to the cost of acquisition hardware. This time-domain signal obtained based on the Nyquist sampling theorem has a large amount of redundant information, and then the workload of feature extraction and analysis for such a huge amount of data has increased exponentially. Therefore, fundamentally reducing the amount of data becomes an urgent problem to be solved by the AE signal fault diagnosis method.

    The CS theory proposed in recent years uses the transform space projection method to realize the compressed sampling of the original signal ADDIN EN.CITE.DATA [8,9,10]. Most of the information contained in the original signal is obtained with very few measured data, thereby greatly improve the data transmission efficiency and reduce the data storage space, which provides a new idea for bearing AE signal fault diagnosis. At present, the bearing fault diagnosis method based on CS has received widespread attention.

    There are many application research of compressed sensing fault diagnosis focus on the optimized feature extraction method. Literature [11] proposed a bearing fault diagnosis method based on CS and matching pursuit (MP) reconstruction algorithm. Literature [12] proposed a CS framework for characteristic harmonics to detect bearing faults. This method uses a compressed MP strategy to detect characteristic harmonics from sparse measurements under the condition of incomplete signal reconstruction. Literature [13] proposed a bearing fault diagnosis method based on CS. This method trains multiple over-complete dictionaries through the dictionary learning method. These dictionaries are effective for the sparse decomposition of signals in each specific state, while signals in other states cannot be sparsely decomposed. This method uses this characteristic to determine the fault state of the bearing. Literature [14] proposed a sparse representation classification strategy, which combined sparse representation with random dimensionality reduction to extract and classify the fault features of rotating machinery. Literature [15] proposed a fault diagnosis method based on sparse representation of time-frequency features, which can reconstruct the time-frequency features of fault signals from a small amount of compressed sampled data containing noise. Literature [16] proposed a method to directly extract the acoustic emission signal compression feature (AECF) from the CS data, and the AECF trend is used to evaluate the running state of the bearing. Literature [22] proposed a fault diagnosis method based on SAE, which combines CS and wavelet packet energy entropy.

    Another hot-spot about compressed sensing fault diagnosis focus on the design classification method. Literature ADDIN EN.CITE [17] uses three methods to process the compressed data and the compressed measured value is directly used as the input of the classifier to diagnose bearing faults. Literature [18] proposed a new intelligent classification method, which uses sparse over-complete features and a deep neural network (DNN) with an unsupervised feature learning algorithm based on sparse autoencoders (SAE) to classify bearing faults in compression measurement. Literature [19] proposed a method for bearing fault diagnosis in a fluctuating environment based on the theory of compressed sensing. The proposed method can effectively reduce the amount of data required for bearing diagnosis and maintain similar accuracy to the current method. Moreover, the reconstructed signal can be used for other fault diagnosis methods. Literature [20] proposed a bearing fault diagnosis method based on CS and heuristic neural networks. Literature ADDIN EN.CITE [21] proposed a new type of intelligent diagnosis method based on CS and deep learning. It uses the advantages of CS and deep learning to obtain high recognition accuracy with a small amount of measurement data.

    The characteristics of bearing fault diagnosis technology based on compression perception above were comprehensively analyzed. Based on the research in reference [16], this paper optimizes and improves the signal decomposition method and feature extraction method in the compressed domain. This method obtains the compressed signal by projecting the signal from the time domain to the compressed domain and is regarded as the original measurement signal; the wavelet packet decomposition of the measured signal is carried out using the wavelet packet change matrix in the compression domain. The characteristic parameters of each frequency band information obtained are taken as feature vectors; the PSO algorithm is used to optimize the weighted coefficient of the feature vector to obtain the fault feature with enhanced feature; the SVM is used to identify and classify bearing fault types. The accuracy and practicability of the method are verified by fault experiments. The contribution of this method is as follows:

    a. A fault diagnosis method combining CS technology and AE signals is proposed. Compressed sampling greatly reduces the amount of AE data and retains most of the effective information of the signal for fault diagnosis. The problem of high hardware requirements for the AE signal due to large data volume is solved.

    b. The transform matrix of wavelet packet decomposition in the compression domain is derived from the time domain wavelet packet decomposition matrix, which is used to perform wavelet packet decomposition of the compression signal. The fault features of the compression domain of different frequency bands are extracted.

    c. Feature weighting is adopted to deal with fault features in the compression domain. The PSO algorithm is used to optimize the weighting coefficient of the fault features. This method realizes the enhancement of weak fault features and avoids the uncertainty of diagnosis results caused by the subjective and one-sided selection of feature information of different frequency bands.

    d. Experimental verification shows that the proposed method has a more satisfactory diagnostic performance for bearing fault diagnosis under low-speed conditions compared with the traditional method.

    CS was proposed by Candes et al. ADDIN EN.CITE.DATA [8,9]. It makes use of the sparse characteristic of signals in a certain transformation domain to compress data while sampling the signal. The compressed data retains most of the information of the original signal, and the reconstruction algorithm uses the observation data to reconstruct the original signal. Most signals in nature are not sparse signals, but a specific transform domain Ψ can be found to make the signal sparse. CS theory points out that if the measured signal xRN is sparse in a certain transform domain Ψ, a measurement matrix ΦRM×N (MN) that is not related to the transform domain can be used to linearly project the measured signal to obtain the compressed signal yRN. Then the original signal ˆx is reconstructed with high probability by solving the optimization problem. The sparse representation of a signal x on the orthogonal basis ΨRN×N is

    x=Ψs (1)

    where the transform coefficient s is sparse and contains only k(kN) non-zero elements. We select the measurement matrix Φ that is not related to Ψ. The signal x is projected to the measurement matrix Φ. Then the reduced-dimensional projection data y is expressed as

    y=Φx=As (2)

    where A=ΦΨ is the perception matrix. To carry out effective and unique signal reconstruction, the expression is often solved by optimizing l1 norm [23] and the greedy algorithm

    ˆx=arg minx1 s.t. As=y (3)

    The signal xRN uses a random measurement matrix Φ of size M×N for compression measurement to obtain compressed data y of size M×1. Then the relationship between the original signal and the compressed data can be expressed as

    (1ε)xy2Φ(xy)2(1+ε)xy2 (4)

    where ε(0,1), the original signal x has approximate distance preserving in Euclidean space before and after projection. Thus, sufficient effective information of the original signal is preserved in the compressed data, which provides a theoretical basis for the feature extraction method of the compressed domain in this paper.

    When the measurement matrix meets the requirement of random projection distance preserving, the signal can be accurately reconstructed. In this paper, the Gaussian random matrix that satisfies the random projection distance preserving property with a high probability is used as the measurement matrix to compress and sample the signal. The measurement matrix is constructed by generating a matrix Φ with the size of M×N, so that each element Φ independently obeys a Gaussian distribution with a mean value of 0 and a variance of 1/1MM [24,25]. This measurement matrix is a random measurement matrix, which is not related to most orthogonal bases or orthogonal dictionaries, and the number of measurements required for accurate reconstruction is small.

    The reduction of signal feature information after original signal compression will affect the effect of subsequent fault diagnosis. This paper proposes a week feature enhancement method for improving the accuracy of fault classification.

    Wavelet packet decomposition can decompose the signal into different frequency bands adaptively, without leakage, and without overlapping according to the feature of the signal. It not only improves the time-frequency resolution of the signal but also obtains more detailed information about the signal. In this paper, wavelet packet transform is used to decompose the compressed signal to extract signal features. The time-domain wavelet packet transform matrix of the original signal xRN is TRN×N, then the decomposition process of the original signal x can be expressed as

    f=Tx (5)

    where fRN is the signal component of the signal x after wavelet packet decomposition in time domain space. Similarly, the wavelet packet transform matrix of the compressed signal yRM is ˆTRM×M, then the decomposition process of the compressed signal is

    ˆf=ˆTy (6)

    where ˆfRM is the signal component of the compressed signal y after the wavelet packet decomposition in the compressed space. According to the distance preserving property of random projection, the dimension reduction observation vector ˆf is obtained by projecting the transformation vector f on the random measurement matrix Φ. Similar to the original signal transformation process, the dimensionality reduction observation vector ˆf is regarded as the compressed data y obtained through signal transformation, then the compressed domain signal transformation can be expressed as ˆf=ˆTy. The premise of analyzing the dimensionality reduction observation vector is to obtain the compression domain transformation matrix ˆT, then the solution formula is

    ˆf=Φf=ΦTx=ˆTΦx (7)
    ˆT=ΦTΦ1 (8)

    In Eq (8), the random measurement matrix Φ is not a square matrix, and the least-squares approximation solution needs to be solved by pseudo-inverse Φ1 so as to solve the transformation matrix ˆT in the compression domain. In this paper, the compression domain transformation matrix is firstly used to decompose the compressed signal, and then the signal features are extracted. As shown in Figure 1, the schematic diagram of the compression domain transformation matrix based on random projection distance preservation is presented. Therefore, the method in this paper can extract the characteristic information of the compressed signal for diagnostic analysis on the premise of ensuring that the compressed signal retains enough effective information of the original signal.

    Figure 1.  Schematic diagram of the compressed domain transformation matrix based on random projection distance preservation.

    The compressed signal is decomposed by wavelet packet to obtain signal features of different frequency bands. Since different frequency bands all contain the local feature information of the signal, if this feature information can be fully utilized, the accuracy of fault classification can be further improved. Therefore, this paper proposes to weight the decomposed signal features, and the PSO method is used to optimize the weight coefficient so as to realize the adaptive selection of the signal features of different frequency bands.

    The PSO algorithm is an intelligent optimization algorithm that tracks the optimal particles in the solution space for searching by simulating the predation behavior of birds. Assuming that there are n particles in the D -dimensional search space, where the position of the i -th particle is Xi=(xi1,xi2,,xiD), and the velocity of the corresponding i -th particle is Vi=(vi1,vi2,,viD). The best position experienced by the i-th particle individual is pbesti=(pi1,pi2,,piD), the best position experienced by the population is gbest=(g1,g2,,gD), then the velocity and position update formula of each particle is

    vk+1id=wvkid+c1r1(pbestidxkid)+c2r2(pbestdxkid) (9)
    xk+1id=xkid+vk+1id (10)

    where w is the inertia weight; c1, c2 are acceleration factors; r1, r2 are random numbers between [0, 1]; d=1,2,,D; i=1,2,,D; k is the current iteration frequency.

    In the optimization process of the particle swarm optimization algorithm, each particle has a fitness function to determine whether the position it has experienced so far is optimal, and then the position is updated after comparison. The distribution of signal feature weight coefficients directly affects the fault classification effect. At this time, it is necessary to ensure that the distance between compressed signal feature classes is as large as possible. Therefore, this paper takes the average distance between compressed signal feature classes as the fitness function, and the expression is as follow

    Di=1n1ni,j=1ijdij (11)

    where Di is the average distance between the i -th type and other classes, dij is the distance between the i -th type feature and the j -th type feature, and n is the number of fault types.

    The particle swarm optimization algorithm steps are as follows:

    Step 1: Initialize the particle swarm and set various parameters.

    Step 2: Evaluate the fitness of each particle according to the fitness function.

    Step 3: Compare the fitness value and update the individual historical best position pbest and the global best position gbest.

    Step 4: Update the position x and velocity v of each particle according to Eqs (9) and (10).

    Step 5: Turn to step 2 to loop iteratively until the number of iterations is satisfied or within the allowable error range, and output the best fitness value and particle position.

    The flow chart of the feature enhancement algorithm based on PSO is shown in Figure 2. When setting the parameters of the particle swarm, the main parameter values are shown in Table 1.

    Figure 2.  Flow chart of feature enhancement algorithm based on PSO.
    Table 1.  PSO algorithm parameter settings.
    Allowable Error The Maximum Number of Iterations Particle Swarm Size n Acceleration Factor c1 Acceleration Factor c2 Inertia Weight
    0.0001 400 700 1.5 1.5 0.8

     | Show Table
    DownLoad: CSV

    By combining CS theory with the PSO algorithm, the problem of AE signal data redundancy can be effectively solved, and the frequency band features containing the main feature information can be adaptively selected to avoid the uncertain influence of subjective parameter setting on experimental results. After the original signal is compressed and sampled, the amount of data is reduced. The compressed signal is decomposed by the wavelet packet in the compressed domain. The PSO algorithm is used to adaptively select the obtained frequency band features, and the fault features are enhanced. Finally, the faults are classified by the SVM. The basic process of bearing AE signal feature enhancement fault diagnosis is shown in Figure 3. The specific steps of the method for enhancing the diagnosis of bearing AE signal weak fault features based on CS are as follows:

    Figure 3.  Flow chart of fault diagnosis for bearing AE signal feature enhancement.

    a. AE signals of different fault states of the rolling bearing are collected by the AE acquisition system to form a data sample set.

    b. The Gaussian random matrix is selected as the measurement matrix Φ. Using Eq (2), the N -dimensional AE signal x is projected to obtain the M -dimensional measurement value y.

    c. The wavelet packet decomposition matrix ˆT in the compressed domain is obtained by Eq (7). The transformation matrix ˆT is used for wavelet packet decomposition of the measured value y. The time domain and frequency domain features of different frequency bands are extracted to form the feature set of the compression domain.

    d. The PSO algorithm is used to calculate the weight of signal features of each frequency band so as to obtain feature sets with sufficient distance between classes.

    e. Input the enhanced feature set into the SVM classifier for training and testing, and finally realize the fault diagnosis of the rolling bearing.

    In order to verify the effectiveness of the method in this paper, thrust ball bearings are used for fault simulation experiments, which simulate three states of normal bearing, raceway failure, and rolling element failure. The ball bearing is installed on the bearing failure simulation test bench, which is composed of six parts: drive device, transmission device, test device, loading device, guide rail device, and anti-overload protection device. AE sensors are used to collect bearing AE signals. The AE acquisition system consists of sensors, preamplifiers, data acquisition cards, hosts, and display. The layout of the test bench and sensors is shown in Figure 4. The experiment uses electrical discharge machining technology to process single-point pits on the central position of the bearing raceway and rolling elements to simulate the weak bearing fault. The corresponding fault diameters are 0.5 mm, 1 mm, 1.5 mm, and the depth is 0.65 mm, as shown in Figure 5. The spindle speed of the test bench is 400 rpm, the preamplifier is set to 60 dB, the sampling frequency is 1 MHz, and the number of data points is 1, 638, 400.

    Figure 4.  Bearing failure test bench.
    Figure 5.  Failure diagram of bearing parts.

    This paper mainly studies the AE signal with reduced data volume after compression. The AE signal is obtained by constructing a Gaussian random measurement matrix and performing random projection compression on it. Figure 6 shows the time domain waveform diagram and frequency spectrum of the AE signal before and after compression of a sample under the three states of normal, race failure, and rolling element failure. It can be seen from Figure 6 that compared with the original AE signal, the compressed AE signals in the three states exhibit relatively similar random characteristics in both the time domain and the frequency domain. The obvious periodic fault features of the original signal cannot be well-reflected. This is due to the loss of some time-domain features of the signal during the compression measurement process. At this time, conventional AE signal analysis methods cannot accurately and effectively perform feature extraction and classification.

    Figure 6.  Time-domain waveforms and spectrograms of three states before and after AE signal compression. (a) Original AE signal waveform; (b) Original AE signal spectrum; (c) Compressed measurement data waveform; (d) Compressed measurement data spectrum.

    Since compressed data shows randomness in amplitude, in order to obtain enough feature information of compressed domain signals, this paper extracts features from compressed data in the time domain and frequency domain. This paper extracts twenty-eight fault features including thirteen-time domain parameters (T1T13) and fifteen-frequency domain parameters (T14T28) from the wavelet packet decomposition components of the compressed data. The specific feature parameter names and calculation formulas are shown in Table 2. T19 and T20 indicate the change of the position of the main frequency band and T21T25 indicate the degree of dispersion or concentration of the spectrum. In Table 2, Xk is the spectrum of signal x, where k=1,2,,N/2.56 is the number of spectral lines, and N is the number of sampling points of signal x. PS[k]=2|XK|2/2|XK|2N2N2, f=2.56fsk/2.56fskNN, M=1+N/N22, P=PS[0]+N/2.56k=1PS[k],

    P0=(N/2.56k=0PS[k]f)/P.
    Table 2.  Characteristic parameter table.
    Serial Number Feature Name Serial Number Feature Name
    T1 Absolute mean T15 Spectral mean
    T2 Mean T16 Spectral skewness index
    T3 Peak index T17 Spectral kurtosis index
    T4 Margin index T18 Root mean square frequency
    T5 Kurtosis index T19 P1
    T6 Skewness index T20 P2
    T7 Zero peak T21 P3
    T8 Impulse indicator T22 P4
    T9 Peak-to-peak T23 P5
    T10 Effective value T24 P6
    T11 Waveform index T25 P7
    T12 Variance T26 Frequency center
    T13 Square root amplitude T27 Spectral variance
    T14 Total spectrum T28 Amplitude spectral entropy
    P1=N/2.56k=0(f2PS[k])P, P2=N/2.56k=0(f2PS[k])PN/2.56k=0(f4PS[k]), P3=1/1MMN/2.56k=0(PS[k]P/PMM)3(1/1MMN/2.56k=0(PS[k]P/PMM)2)3, P4=1/1MMN/2.56k=0(PS[k]P/PMM)4(1/1MMN/2.56k=0(PS[k]P/PMM)2)2, P5=2.56N/2.56k=0((fP0)2PS[k])N, P6=P5P0, P7=N/2.56k=0((fp0)3PS[k])P5

     | Show Table
    DownLoad: CSV

    According to the feature enhancement method in this article, firstly, the AE data of different states are obtained. Two hundred sets of data are taken from each state, and 8192 sample points are intercepted from each set of data. Secondly, the AE data is compressed and measured, and a total of 600 sets of data are compressed and projected to obtain compressed data with a length of 4096 (downsampling rate R=2). Then feature extraction is carried out for the compressed domain data. According to experience, three-layer wavelet packet decomposition is selected, and each group of sample signals will generate 8 component signals of different frequency bands so that there are 4800 component signals of 600 × 8. Twenty-eight eigenvalues of each group of sample wavelet packet decomposition data are calculated to obtain an eigenmatrix of the sample signal compression domain with a size of 4800 × 28. Finally, most of the multi-component signals of these compressed data contain low-frequency information and high-frequency noise signals of bearing operation, and the fault information contained therein is masked, which has a strong interference effect on fault identification. Therefore, in order to improve the classification accuracy of compressed data, weaken the interference of high-frequency noise, and enhance the weak fault characteristic signal, the PSO method can be used to optimize the characteristic weight coefficients of the eight components of the wavelet packet decomposition of each sample to realize the characteristic enhancement and obtain a 600 × 28 eigenvalue matrix.

    One feature that is relatively obvious in comparison among the three sample data is selected. As shown in Figure 7, the signal feature is extracted directly after compression and the Characteristic parameters of the signal after the fault feature is enhanced. It can be seen from Figure 7(a) that the compressed feature parameters are in disorder and difficult to classify. In Figure 7(b), the compressed signal is decomposed by wavelet packet by the method of this paper, and the features of each compon-ent signal are extracted for weighted summation. It can be seen that the characteristic parameters of different types of faults obviously have certain laws. Normal and faulty bearings are effectively separated. The two faults of the raceway and rolling element are relatively poor, but they can still be clearly identified. This paper takes different types of fault features as input and selects a suitable proportion of training set and test set. The fault type and classification accuracy are determined by the matching degree of training set prediction classification and test set classification.

    Figure 7.  Comparison of features extracted directly from compressed domain and feature parameters after feature enhancement. (a) Compressed domain feature parameters; (b) Feature parameters after fault feature enhancement.

    The feature set is formed by feature extraction and enhancement of the compressed data, and the feature vector matrix is divided into the training set and the test set by 4:1. The kernel function of SVM selects the Gaussian radial basis function, and the results of classification using this method are shown in Table 3. It can be seen from Table 3 that the data samples are divided into three categories. The test sample numbers 1–40, 41–80, 81–120 are a group of samples corresponding to normal, race failure, and rolling element failure. The 120 samples in the test set use the weak fault feature enhancement algorithm to accurately identify various fault samples with a classification accuracy of 100%.

    Table 3.  Classification results of different types of faults.
    Fault Type Speed/rpm Fault Diameter/mm Sample Number Classification Accuracy Rate/%
    Normal 400 0 1-200 100
    Race failure 400 0.5 201-400 100
    rolling element failure 400 0.5 401-600 100

     | Show Table
    DownLoad: CSV

    In order to further verify the effectiveness of the method in this paper, the different faults of bearing races and rolling elements are diagnosed. When the spindle speed is 400 rpm, the diameter of the race failure and the rolling element failure are respectively 0.5 mm, 1 mm and 1.5 mm. There are three types of failure samples. The specific parameter settings are shown in Table 4. After the same compression measurement, three-layer wavelet packet decomposition, feature enhancement, and classification process, the ratio of the training set to the test set is 4:1. The experimental characteristic parameters of different degrees of failure before and after the compression domain feature enhancement are shown in Figure 8. It can be seen from Figure 8(a) and (c) that feature extraction is conducted on the compressed data obtained from the race fault degree experiment and the rolling element fault degree experiment, and the characteristic parameters of different fault types are all mixed, irregular and difficult to separate. From Figure 8(b) and (d), it can be seen that the feature parameters of different fault levels obtained by the feature enhancement method of the PSO algorithm to optimize the weight coefficients show more regularity, better classification and recognition, and larger class spacing. So as to provide more accurate classification information for subsequent bearing fault diagnosis and greatly improve the accuracy of diagnosis. The classification results of the fault feature enhancement diagnosis method are shown in Table 5. The weak fault feature enhancement method based on the proposed method can accurately identify faults of different degrees with 100% classification accuracy for different experimental types. Therefore, the four different degrees of race faults and rolling element faults can be accurately identified with 100% classification accuracy for fault diagnosis using this method.

    Table 4.  Different degrees of seat ring/rolling element failure parameter table.
    Fault State Speed/rpm Fault Diameter/mm Sample Number
    Race/rolling element failure degree 400 0 1–200
    400 0.5 201–400
    400 1 401–600
    400 1.5 601–800

     | Show Table
    DownLoad: CSV
    Figure 8.  Compressed domain features of different experimental types enhance the front and back feature parameters. (a) Feature parameters directly extracted from race faults; (b) Feature parameters after enhanced race fault features; (c) Feature parameters directly extracted from rolling element faults; (d) Feature parameters after enhanced rolling element fault features.
    Table 5.  Classification results of different degrees of seat/rolling element failure.
    Experiment Type Training Samples Test Sample Identify the Sample Diagnostic Accuracy Rate/%
    Race failure degree test 640 160 160 100
    Rolling element failure degree experiment 640 160 160 100

     | Show Table
    DownLoad: CSV

    Through the verification of experimental data, we can see that the fault diagnosis method in this paper has obtained perfect results. It can not only correctly classify various faults but also identify different degrees of faults, and the recognition accuracy of each fault can reach 100%. It shows that the method proposed in this paper is effective, which can accurately diagnose different types of bearing faults while reducing the amount of data.

    The compression rate reflects the degree of compression of the original signal. Restricted by the constrained equidistance condition, an excessively large compression rate under the condition of a limited number of sampling points will cause serious information loss of the compressed signal. The signal reconstruction error of the normal bearing AE signal under different compression ratios is shown in Figure 9. It can be seen that as the compression rate increases, the reconstruction error of the signal gradually increases, and the reconstruction error is basically in the range of 30 to 50%. When the compression ratio is in the range of 2–4, the OMP method can obtain a smaller reconstruction error, and the reconstruction effect has become better. When the compression ratio is greater than 10, the reconstruction error is large, and the feature information in the compressed data is greatly reduced.

    Figure 9.  Signal reconstruction errors under different compression rates.

    Discrete Cosine Transform (DCT) is an orthogonal projection transformation method that transforms a signal from the time domain to the frequency domain. The key information of the signal is mainly concentrated on a few low-frequency coefficients. DCT is suitable for sparse representation of local singular parts and has a good effect on sparse representation of low-frequency parts. It has strong energy concentration characteristics and decorrelation performance and has good robustness to noise. The Orthogonal Match Pursuit (OMP) algorithm is an iterative greedy algorithm and a classic algorithm for solving the l1 norm. The algorithm calculates the current optimal solution in each iteration, updates the residuals, and finds the optimal global solution through continuous iterations. The calculation speed is fast, and it is easy to implement. It is very suitable for signal reconstruction.

    According to the above analysis, the DCT method is used to sparsely represent the original AE signal, the OMP method is used to reconstruct the signal, and the compression rate R = 2 is selected to reconstruct the original signal. The signal reconstruction error is 0.31, and the signal-to-noise ratio is 5, indicating that the reconstruction method using CS can restore the original signal more accurately. Therefore, the effective key information in the original signal is retained in the compressed measurement data, and the original signal can be reconstructed with a lower reconstruction error. This provides sufficient feature information for feature extraction in the compressed domain.

    In order to further verify the effect of the bearing AE signal fault feature enhancement method based on CS, we selected several bearing fault diagnosis methods to compare with the method in this paper. Mainly include: a) Input the compressed data directly into the neural network and use the Softmax classifier to classify; b) Extract the features from the compressed data and input the support vector machine; c) The original AE signal input the support vector machine after extracting the features. Under the conditions of the same parameters, the classification accuracy of the four bearing AE signal fault diagnosis methods is shown in Figure 10.

    Figure 10.  Classification results of different methods under three experimental types.

    It can be seen from Figure 10 that four-fault diagnosis methods are used for different degrees of seat ring failure, different degrees of rolling element failure, and different types of failures. The method in this paper has high diagnostic efficiency in the three types of experiments. The accuracy rate reaches 100%, which can realize accurate diagnosis of different fault states. The accuracy of the compressed data input neural network method is low under the three experimental conditions; the method of direct classification of compressed domain feature extraction has the lowest diagnostic accuracy, and the lowest is only 57.5%; the diagnostic accuracy of the method of extracting features from the original AE signals for classification is relatively high, up to 96.67%, but fluctuates greatly under different experiments. In summary, compared with the traditional methods, the method in this paper has obvious advantages by enhancing the weak fault characteristics after CS. No matter in terms of diagnostic accuracy and the wide applicability and stability of the diagnostic method, the method in this paper shows good results.

    The reason why the method in this paper is superior to other methods is that the processing object of this paper is to compress the signal, and the less signal contains most of the characteristic information of the original time-domain signal. Then the weak fault features of the compressed signal can be enhanced by some adaptive selection of frequency band information, and the classification accuracy can be higher with fewer data; however, the traditional signal classification method based on time-frequency statistical feature parameters cannot accurately obtain all the information of the signal, so the diagnosis accuracy rate is low when combined with the SVM classifier; in addition, the compression signal classification method based on neural network is limited by the number of hidden layers, the number of training samples and the training method, resulting in unstable network performance and low diagnostic recognition rate.

    Aiming at the problems of high cost and difficulty in data processing caused by a large amount of data transmission in the fault diagnosis of bearing AE signal, this paper proposes an enhanced diagnosis method for weak fault features of bearing AE signal based on CS. The method presented in this paper is successfully applied to the fault diagnosis of rolling bearings under the condition of ensuring high diagnostic accuracy. The method directly deals with the AE signal in the compression domain of the rolling bearing fault. The wavelet packet decomposition and the PSO method are used to realize the intelligent selection of frequency bands with more fault feature information. It not only solves the problem of the large data volume of AE signal data processing in fault diagnosis but also solves the problem of weak fault characteristics of compressed data. The signal appears in a random and disordered state in the compressed domain. The components decomposed by wavelet packet contain a large amount of feature information. The method of adaptive feature weighting is used to extract effective and enhanced fault information, which avoids the blindness of component selection. The effectiveness of the proposed fault feature enhancement diagnosis method is verified by bearing fault experiments. The method in this paper can accurately identify different types of faults and different degrees of faults. The appropriate compression ratio is selected through the reconstruction error curve of the compression ratio so as to prove that the compression domain signal has enough feature information, and ensure the effectiveness of feature enhancement and the accuracy of fault diagnosis. Finally, compared with the other three traditional fault diagnosis methods, the method in this paper has better performance in terms of the stability of diagnosis and the accuracy of recognition. The method proposed in this paper provides a new idea for the fault diagnosis of compressed signal processing. At the same time, it provides a new diagnosis method for equipment fault diagnosis under big modern data, which has a high engineering application value.

    This work was supported in part by the National Key R & D Program of China under Awards 2018YFB1306100 and in part by the National Natural Science Foundation of China under Awards 51875272 and in part by Kunming University of Science and Technology Scientific Research Start-up Fund for Talents Introduction under Awards KK23201801048, and in part by Yunnan Provincial School Education Cooperation Key Project under Awards KKDA202001003.

    The authors declare no conflict of interest.


    Abbreviation FasL: Fas ligand; FasLECD: Fas ligand extracellular domain; FasR: Fas receptor; FasRECD: Fas receptor extracellular domain; FasR-mAb: anti-Fas receptor extracellular-domain monoclonal-antibody; sFasL: soluble Fas ligand; mFasL: cell-surface membrane-bound Fas ligand;
    Acknowledgments



    This work was supported by a grant for operating expenses from the Ministry of Economy, Trade and Industry, Japan. The author thanks all of the members of National Institute of Advanced Industrial Science and Technology, Japan, especially Dr. Kiyonori Hirota, for their assistance in publishing this paper.

    Conflict of interest



    The author declares no conflict of interest in this paper.

    [1] Walczak H (2013) Death receptor-ligand systems in cancer, cell death, and inflammation. Cold Spring Harb Perspect Biol 5: a008698. doi: 10.1101/cshperspect.a008698
    [2] Calmon-Hamaty F, Audo R, Combe B, et al. (2015) Targeting the Fas/FasL system in rheumatoid arthritis therapy: promising or risky? Cytokine 75: 228-233. doi: 10.1016/j.cyto.2014.10.004
    [3] Franke DDH, Yolcu ES, Alard P, et al. (2007) A novel multimeric form of FasL modulates the ability of diabetogenic T cells to mediate type 1 diabetes in an adoptive transfer model. Mol Immunol 44: 2884-2892. doi: 10.1016/j.molimm.2007.01.014
    [4] Nagata S (1997) Apoptosis by death factor. Cell 88: 355-365. doi: 10.1016/S0092-8674(00)81874-7
    [5] Muraki M (2018) Development of expression systems for the production of recombinant human Fas ligand extracellular domain derivatives using Pichia pastoris and preparation of the conjugates by site-specific chemical modifications: A review. AIMS Bioengineer 5: 39-62. doi: 10.3934/bioeng.2018.1.39
    [6] Powell WC, Fingleton B, Wilson CL, et al. (1999) The metalloproteinase matrilysin proteolytically generates active soluble Fas ligand and potentiates epithelial cell apoptosis. Curr Biol 9: 1441-1447. doi: 10.1016/S0960-9822(00)80113-X
    [7] Mitsiades N, Yu WH, Poulaki V, et al. (2001) Matrix metalloproteinase-7-mediated cleavage of Fas ligand protects tumor cells from chemotherapeutic drug cytotoxicity. Cancer Res 61: 577-581.
    [8] Schneider P, Holler N, Bodmer JL, et al. (1998) Conversion of membrane-bound Fas (CD95) ligand to its soluble form is associated with downregulation of its proapoptotic activity and loss of liver toxicity. J Exp Med 187: 1205-1213. doi: 10.1084/jem.187.8.1205
    [9] Tanaka M, Suda T, Takahashi T, et al. (1995) Expression of functional soluble form of human Fas ligand in activated lymphocytes. EMBO J 14: 1129-1135. doi: 10.1002/j.1460-2075.1995.tb07096.x
    [10] Herrero R, Kajikawa O, Matute-Bello G, et al. (2011) The biological activity of FasL in human and mouse lungs is determined by the structure of its stalk region. J Clin Invest 121: 1174-1190. doi: 10.1172/JCI43004
    [11] Tanaka M, Itai T, Adachi M, et al. (1998) Downregulation of Fas ligand by shedding. Nature Med 4: 31-36. doi: 10.1038/nm0198-031
    [12] Matsumoto H, Murakami Y, Kataoka K, et al. (2015) Membrane-bound and soluble Fas ligands have opposite functions in photoreceptor cell death following separation from the retinal pigment epithelium. Cell Death Dis 6: e1986. doi: 10.1038/cddis.2015.334
    [13] Suda T, Hashimoto H, Tanaka M, et al. (1997) Membrane Fas ligand kills human peripheral blood T lymphocytes, and soluble Fas ligand blocks the killing. J Exp Med 186: 2045-2050. doi: 10.1084/jem.186.12.2045
    [14] Audo R, Calmon-Hamaty F, Papon L, et al. (2014) Distinct effects of soluble and membrane-bound Fas ligand on fibroblast-like synoviocytes from rheumatoid arthritis patients. Arthritis Rheum 66: 3289-3299. doi: 10.1002/art.38806
    [15] Song E, Chen J, Ouyang N, et al. (2001) Soluble Fas ligand released by colon adenocarcinoma cells induces host lymphocyte apoptosis: an active mode of immune evasion in colon cancer. Br J Cancer 85: 1047-1054. doi: 10.1054/bjoc.2001.2042
    [16] Wadsworth SJ, Atsuta R, McIntyre JO, et al. (2010) IL-13 and TH2 cytokine exposure triggers matrix metalloproteinase 7-mediated Fas ligand cleavage from bronchial epithelial cells. J Allergy Clin Immnunol 126: 366-374. doi: 10.1016/j.jaci.2010.05.015
    [17] Soni H, Kaminski D, Gangaraju R, et al. (2018) Cisplatin-induced oxidative stress stimulates renal Fas ligand shedding. Renal Failure 40: 314-322. doi: 10.1080/0886022X.2018.1456938
    [18] Lotti R, Shu E, Petrachi T, et al. (2018) Soluble Fas ligand is essential for blister formation in pemphigus. Front Immunol 9: 370. doi: 10.3389/fimmu.2018.00370
    [19] Komada Y, Inaba H, Li QS, et al. (1999) Epitopes and functional responses defined by a panel of anti-Fas (CD95) monoclonal antibodies. Hybridoma 18: 391-398. doi: 10.1089/hyb.1999.18.391
    [20] Chodorge M, Züger S, Stirnimann C, et al. (2012) A series of Fas receptor agonist antibodies that demonstrate an inverse correlation between affinity and potency. Cell Death Differ 19: 1187-1195. doi: 10.1038/cdd.2011.208
    [21] Shiraishi T, Suzuyama K, Okamoto H, et al. (2004) Increased cytotoxicity of soluble Fas ligand by fusing isoleucine zipper motif. Biochem Biophys Res Comm 322: 197-202. doi: 10.1016/j.bbrc.2004.07.098
    [22] Daburon S, Devaud C, Costet P, et al. (2013) Functional characterization of a chimeric soluble Fas ligand polymer with in vivo anti-tumor activity. Plos One 8: e54000. doi: 10.1371/journal.pone.0054000
    [23] Cremesti A, Paris F, Grassme H, et al. (2001) Ceramide enables Fas to cap and kill. J Biol Chem 276: 23954-23961. doi: 10.1074/jbc.M101866200
    [24] Muraki M (2014) Improved production of recombinant human Fas ligand extracellular domain in Pichia pastoris: yield enhancement using disposable culture-bag and its application to site-specific chemical modifications. BMC Biotechnol 14: 19. doi: 10.1186/1472-6750-14-19
    [25] Wajant H, Gerspach J, Pfizenmaier K (2013) Engineering death receptor ligands for cancer therapy. Cancer Lett 332: 163-174. doi: 10.1016/j.canlet.2010.12.019
    [26] Muraki M, Hirota K (2017) Site-specific chemical conjugation of human Fas ligand extracellular domain using trans-cyclooctene–methyltetrazine reactions. BMC Biotechnol 17: 56. doi: 10.1186/s12896-017-0381-2
    [27] Herrmann T, Große-Hovest L, Otz T, et al. (2008) Construction of optimized bispecific antibodies for selective activation of the death receptor CD95. Cancer Res 68: 1221-1227. doi: 10.1158/0008-5472.CAN-07-6175
    [28] Kaplan DH, Shankaran V, Dighe AS, et al. (1998) Demonstration of an interferon γ-dependent tumor surveillance system in immunocompetent mice. Proc Natl Acad Sci USA 95: 7556-7561. doi: 10.1073/pnas.95.13.7556
    [29] Gravett AM, Dalgleish AG, Copier J (2019) In vitro culture with gemcitabine augments death receptor and NKG2D ligand expression on tumour cells. Sci Rep 9: 1544. doi: 10.1038/s41598-018-38190-2
    [30] Micheau O, Solary E, Hammann A, et al. (1997) Sensitization of cancer cells treated with cytotoxic drugs to Fas-mediated cytotoxicity. J Natl Cancer Inst 89: 783-789. doi: 10.1093/jnci/89.11.783
    [31] Micheau O, Solary E, Hammann A, et al. (1999) Fas ligand-independent, FADD-mediated activation of the Fas death pathway by anticancer drugs. J Biol Chem 274: 7987-7992. doi: 10.1074/jbc.274.12.7987
    [32] Micheau O, Hammann A, Solary E, et al. (1999) STAT-1-independent upregulation of FADD and procaspase-3 and -8 in cancer cells treated with cytotoxic drugs. Biochem Biophys Res Comm 256: 603-607. doi: 10.1006/bbrc.1999.0391
    [33] Petak I, Tillman DM, Houghton JA (2000) p53 dependence of Fas induction and acute apoptosis in response to 5-fluorouracil-leucovorin in human colon carcinoma cell lines. Clin Cancer Res 6: 4432-4441.
    [34] Bergmann-Leitner ES, Abrams SI (2001) Treatment of human colon cell lines with anti-neoplastic agents enhances their lytic sensitivity to antigen-specific CD8+ cytotoxic T lymphocytes. Cancer Immunol Immunother 50: 445-455. doi: 10.1007/s002620100229
    [35] van Geelen CMM, de Vries EGE, Le TKP, et al. (2003) Differential modulation of the TRAIL receptors and the CD95 receptor in colon carcinoma cell lines. Br J Cancer 89: 363-373. doi: 10.1038/sj.bjc.6601065
    [36] Lacour S, Micheau O, Hammann A, et al. (2003) Chemotherapy enhances TNF-related apoptosis-inducing ligand DISC assembly in HT29 human colon cancer cells. Oncogene 22: 1807-1816. doi: 10.1038/sj.onc.1206127
    [37] Dong YB, Yang HL, McMasters KM (2003) E2F-1 overexpression sensitizes colorectal cancer cells to camptothecin. Cancer Gene Ther 10: 168-178. doi: 10.1038/sj.cgt.7700565
    [38] Lacour S, Hammann A, Grazide S, et al. (2004) Cisplatin-induced CD95 redistribution into membrane lipid rafts of HT29 human colon cancer cells. Cancer Res 64: 3593-3598. doi: 10.1158/0008-5472.CAN-03-2787
    [39] McDermott U, Longley DB, Galligan L, et al. (2005) Effect of p53 status and STAT1 on chemotherapy-induced, Fas-mediated apoptosis in colorectal cancer. Cancer Res 65: 8951-8960. doi: 10.1158/0008-5472.CAN-05-0961
    [40] Lin HH, Shi MD, Tseng HC, et al. (2014) Andrographolide sensitizes the cytotoxicity of human colorectal carcinoma cells toward cisplatin via enhancing apoptosis pathways in vitro and in vivoToxicol Sci 139: 108-120. doi: 10.1093/toxsci/kfu032
    [41] Pace E, Melis M, Siena L, et al. (2000) Effects of gemcitabine on cell proliferation and apoptosis in non-small-cell lung cancer (NSCLC) cell lines. Cancer Chemother Pharmacol 46: 467-476. doi: 10.1007/s002800000183
    [42] Supino R, Perego P, Gatti L, et al. (2001) A role for c-myc in DNA damage-induced apoptosis in a human TP53-mutant small-cell lung cancer cell line. Eur J Cancer 37: 2247-2256. doi: 10.1016/S0959-8049(01)00268-4
    [43] Okouoyo S, Herzer K, Ucur E, et al. (2004) Rescue of death receptor and mitochondrial apoptosis signaling in resistant human NSCLC in vivoInt J Cancer 108: 580-587. doi: 10.1002/ijc.11585
    [44] Yoshimoto Y, Kawada M, Ikeda D, et al. (2005) Involvement of doxorubicin-induced Fas expression in the antitumor effect of doxorubicin on Lewis lung carcinoma in vivoInt Immunopharmacol 5: 281-288. doi: 10.1016/j.intimp.2004.09.032
    [45] Li Y, Xing D, Chen Q, et al. (2010) Enhancement of chemotherapeutic agent-induced apoptosis by inhibition of NF-κB using ursolic acid. Int J Cancer 127: 462-473.
    [46] Siena L, Pace E, Ferraro M, et al. (2013) Gemcitabine sensitizes lung cancer cells to Fas/FasL system-mediated killing. Immunology 141: 242-255. doi: 10.1111/imm.12190
    [47] Wang LH, Li Y, Yang SN, et al. (2014) Gambogic acid synergistically potentiates cisplatin-induced apoptosis in non-small-cell lung cancer through suppressing NF-κB and MAPK/HO-1 signaling. Br J Cancer 110: 341-352. doi: 10.1038/bjc.2013.752
    [48] Weller M, Winter S, Schmidt C, et al. (1997) Topoisomerase-I inhibitors for human malignant glioma: differential modulation of p53, p21, bax, and bcl-2 expression and of CD95-mediated apoptosis by camptothecin and β-lapachone. Int J Cancer 73: 707-714. doi: 10.1002/(SICI)1097-0215(19971127)73:5<707::AID-IJC16>3.0.CO;2-2
    [49] Fulda S, Lutz W, Schwab M, et al. (1999) MycN sensitizes neuroblastoma cells for drug-induced apoptosis. Oncogene 18: 1479-1486. doi: 10.1038/sj.onc.1202435
    [50] Ciusani E, Perego P, Carenini N, et al. (2002) Fas/CD95-mediated apoptosis in human glioblastoma cells: a target for sensitization to topoisomerase I inhibitors. Biochem Pharmacol 63: 881-887. doi: 10.1016/S0006-2952(01)00837-1
    [51] Bian X, Giordano TD, Lin HJ, et al. (2004) Chemotherapy-induced apoptosis of S-type neuroblastoma cells requires caspase-9 and is augmented by CD95/Fas stimulation. J Biol Chem 279: 4663-4669. doi: 10.1074/jbc.M306905200
    [52] Terrasson J, Allart S, Martin H, et al. (2005) p73-dependent apoptosis through death receptor: impairment by human cytomegalovirus infection. Cancer Res 65: 2787-2794. doi: 10.1158/0008-5472.CAN-04-2019
    [53] Xia S, Rosen EM, Laterra J (2005) Sensitization of glioma cells to Fas-dependent apoptosis by chemotherapy-induced oxidative stress. Cancer Res 65: 5248-5255. doi: 10.1158/0008-5472.CAN-04-4332
    [54] Galenkamp KMO, Carriba P, Urresti J, et al. (2015) TNFα sensitizes neuroblastoma cells to FasL-, cisplatin- and etoposide-induced cell death by NF-κB-mediated expression of Fas. Mol Cancer 14: 62. doi: 10.1186/s12943-015-0329-x
    [55] Uslu R, Jewett A, Bonavida B (1996) Sensitization of human ovarian tumor cells by subtoxic CDDP to anti-Fas antibody-mediated cytotoxicity and apoptosis. Gynecol Oncol 62: 282-291. doi: 10.1006/gyno.1996.0228
    [56] Uslu R, Borsellino N, Frost P, et al. (1997) Chemosensitization of human prostate carcinoma cell lines to anti-Fas-mediated cytotoxicity and apoptosis. Clin Cancer Res 3: 963-972.
    [57] Mansouri A, Ridgway LD, Korapati A, et al. (2003) Sustained activation of JNK/p38 MAPK pathways in response to cisplatin leads to Fas ligand induction and cell death in ovarian carcinoma cells. J Biol Chem 278: 19245-19256. doi: 10.1074/jbc.M208134200
    [58] Bagnoli M, Balladore E, Luison E, et al. (2007) Sensitization of p53-mutated epithelial ovarian cancer to CD95-mediated apoptosis is synergistically induced by cisplatin pretreatment. Mol Cancer Ther 6: 762-772. doi: 10.1158/1535-7163.MCT-06-0357
    [59] Alagkiozidis I, Facciabene A, Carpenito C, et al. (2009) Increased immunogenicity of surviving tumor cells enables cooperation between liposomal doxorubicin and IL-18. J Transl Med 7: 104. doi: 10.1186/1479-5876-7-104
    [60] Karaca B, Atmaca H, Bozkurt E, et al. (2013) Combination of AT-101/cisplatin overcomes chemoresistance by inducing apoptosis and modulating epigenetics in human ovarian cancer cells. Mol Biol Rep 40: 3925-3933. doi: 10.1007/s11033-012-2469-z
    [61] Frost P, Ng CP, Belldegrun A, et al. (1997) Immunosensitization of prostate carcinoma cell lines for lymphocytes (CTL, TIL, LAK)-mediated apoptosis via the Fas-Fas-ligand pathway of cytotoxicity. Cell Immunol 180: 70-83. doi: 10.1006/cimm.1997.1169
    [62] Costa-Pereira AP, Cotter TG (1999) Camptothecin sensitizes androgen-independent prostate cancer cells to anti-Fas-induced apoptosis. Br J Cancer 80: 371-378. doi: 10.1038/sj.bjc.6690365
    [63] Costa-Pereira AP, McKenna SL, Cotter TG (2000) Activation of SAPK/JNK by camptothecin sensitizes androgen-independent prostate cancer cells to Fas-induced apoptosis. Br J Cancer 82: 1827-1834. doi: 10.1054/bjoc.2000.1149
    [64] Frost PJ, Butterfield LH, Dissette VB, et al. (2001) Immunosensitization of melanoma tumor cells to non-MHC Fas-mediated killing by MART-1-specific CTL cultures. J Immunol 166: 3564-3573. doi: 10.4049/jimmunol.166.5.3564
    [65] Das A, Durrant D, Mitchell C, et al. (2015) Sildenafil (Viagra) sensitizes prostate cancer cells to doxorubicin-mediated apoptosis through CD95. Oncotarget 7: 4399-4413. doi: 10.18632/oncotarget.6749
    [66] Ruiz-Ruiz MC, López-Rivas A (1999) p53-mediated up-regulation of CD95 is not involved in genotoxic drug-induced apoptosis of human breast tumor cells. Cell Death Differ 6: 271-280. doi: 10.1038/sj.cdd.4400490
    [67] Ruiz-Ruiz C, Muñoz-Pinedo C, López-Rivas A (2000) Interferon-γ treatment elevates caspase-8 expression and sensitizes human breast tumor cells to a death receptor-induced mitochondria-operated apoptotic program. Cancer Res 60: 5673-5680.
    [68] Basma H, El-Refaey H, Sgagias MK, et al. (2005) Bcl-2 antisense and cisplatin combination treatment of MCF-7 breast cancer cells with or without functional p53. J Biomed Sci 12: 999-1011. doi: 10.1007/s11373-005-9025-y
    [69] Mohammad N, Singh SV, Malvi P, et al. (2015) Strategy to enhance efficacy of doxorubicin in solid tumor cells by methyl-β-cyclodextrin: involvement of p53 and Fas receptor ligand complex. Sci Rep 5: 11853. doi: 10.1038/srep11853
    [70] Posovszky C, Friesen C, Herr I, et al. (1999) Chemotherapeutic drugs sensitize pre-B ALL cells for CD95- and cytotoxic T-lymphocyte-mediated apoptosis. Leukemia 13: 400-409. doi: 10.1038/sj.leu.2401327
    [71] Ortiz-Lazareno PC, Bravo-Cuellar A, Lerma-Díaz JM, et al. (2014) Sensitization of U937 leukemia cells to doxorubicin by the MG132 proteasome inhibitor induces an increase in apoptosis by suppressing NF-kappa B and mitochondrial membrane potential loss. Cancer Cell Int 14: 13. doi: 10.1186/1475-2867-14-13
    [72] Duverger V, Sartorius U, Klein-Bauernschmitt P, et al. (2002) Enhancement of cisplatin-induced apoptosis by infection with adeno-associated virus type 2. Int J Cancer 97: 706-712. doi: 10.1002/ijc.10077
    [73] Lim YS, So HS, Kim MS, et al. (2002) Palgin sensitizes the Adriamycin-induced apoptosis via the enhancement of Fas/Fas ligand expression. Life Sci 71: 2391-2401. doi: 10.1016/S0024-3205(02)02039-8
    [74] Hougardy BMT, van der Zee AGJ, van den Heuvel FAJ, et al. (2005) Sensitivity to Fas-mediated apoptosis in high-risk HPV-positive human cervical cancer cells: relationship with Fas, caspase-8, and Bid. Gynecol Oncol 97: 353-364. doi: 10.1016/j.ygyno.2005.01.036
    [75] Sui Y, Yang Y, Wang J, et al. (2015) Lysophosphatidic acid inhibits apoptosis induced by cisplatin in cervical cancer cells. BioMed Res Int 2015: 598386.
    [76] Kinoshita H, Yoshikawa H, Shiiki K, et al. (2000) Cisplatin (CDDP) sensitizes human osteosarcoma cell to Fas/CD95-mediated apoptosis by down-regulating FLIP-L expression. Int J Cancer 88: 986-991. doi: 10.1002/1097-0215(20001215)88:6<986::AID-IJC23>3.0.CO;2-B
    [77] Yuan XW, Zhu XF, Huang XF, et al. (2007) p14ARF sensitizes human osteosarcoma cells to cisplatin-induced apoptosis in a p53-independent manner. Cancer Biol Ther 6: 1074-1080. doi: 10.4161/cbt.6.7.4324
    [78] Huang T, Gong WH, Zou CP, et al. (2014) Marsdenia tenacissima extract sensitizes MG63 cells to doxorubicin-induced apoptosis. Genet Mol Res 13: 354-362. doi: 10.4238/2014.January.21.3
    [79] Pei Q, Pan J, Ding X, et al. (2015) Gemcitabine sensitizes pancreatic cancer cells to the CTLs antitumor response induced by BCG-stimulated dendritic cells via a Fas-dependent pathway. Pancreatology 15: 233-239. doi: 10.1016/j.pan.2015.04.001
    [80] Pietkiewicz S, Eils R, Krammer PH, et al. (2015) Combinatorial treatment of CD95L and gemcitabine in pancreatic cancer cells induces apoptotic and RIP1-mediated necroptotic cell death network. Exp Cell Res 339: 1-9. doi: 10.1016/j.yexcr.2015.10.005
    [81] Yang S, Haluska FG (2004) Treatment of melanoma with 5-fluorouracil or dacarbazine in vitro sensitizes cells to antigen-specific CTL lysis through perforin/granzyme- and Fas-mediated pathways. J Immunol 172: 4599-4608. doi: 10.4049/jimmunol.172.7.4599
    [82] Wu XX, Mizutani Y, Kakehi Y, et al. (2000) Enhancement of Fas-mediated apoptosis in renal cell carcinoma cells by adriamycin. Cancer Res 60: 2912-2818.
    [83] Kuwahara D, Tsutsumi K, Kobayashi T, et al. (2000) Caspase-9 regulates cisplatin-induced apoptosis in human head and neck squamous cell carcinoma cells. Cancer Lett 148: 65-71. doi: 10.1016/S0304-3835(99)00315-8
    [84] Kataoka T, Ito M, Budd RC, et al. (2002) Expression level of c-FILP versus Fas determines susceptibility to Fas ligand-induced cell death in murine thymoma EL-4 cells. Exp Cell Res 273: 256-264. doi: 10.1006/excr.2001.5438
    [85] Iwase M, Watanabe H, Kondo G, et al. (2003) Enhanced susceptibility of oral squamous cell carcinoma cell lines to Fas-mediated apoptosis by cisplatin and 5-fluorouracil. Int J Cancer 106: 619-625. doi: 10.1002/ijc.11239
    [86] Spierings DCJ, de Vries EGE, Stel AJ, et al. (2004) Low p21Waf1/Cip1 protein level sensitizes testicular germ cell tumor cells to Fas-mediated apoptosis. Oncogene 23: 4862-4872. doi: 10.1038/sj.onc.1207617
    [87] Yamana K, Bilim V, Hara N, et al. (2005) Prognostic impact of Fas/CD95/APO-1 in urothelial cancers: decreased expression of Fas is associated with disease progression. Br J Cancer 93: 544-551. doi: 10.1038/sj.bjc.6602732
    [88] Nitobe J, Yamaguchi S, Okuyama M, et al. (2003) Reactive oxygen species regulate FLICE inhibitory protein (FLIP) and susceptibility to Fas-mediated apoptosis in cardiac myocytes. Cardiovasc Res 57: 119-128. doi: 10.1016/S0008-6363(02)00646-6
    [89] Labroille G, Dumain P, Lacombe F, et al. (2000) Flow cytometric evaluation of fas expression in relation to response and resistance to anthracyclines in leukemic cells. Cytometry 39: 195-202. doi: 10.1002/(SICI)1097-0320(20000301)39:3<195::AID-CYTO4>3.0.CO;2-A
    [90] Fulda S, Küfer MU, Meyer E, et al. (2001) Sensitization for death receptor- or drug-induced apoptosis by re-expression of caspase-8 through demethylation or gene transfer. Oncogene 20: 5865-5877. doi: 10.1038/sj.onc.1204750
    [91] Yang D, Torres CM, Bardhan K, et al. (2012) Decitabine and vorinostat cooperate to sensitize colon carcinoma cells to Fas ligand-induced apoptosis in vitro and tumor suppression in vivoJ Immunol 188: 4441-4449. doi: 10.4049/jimmunol.1103035
    [92] Mishima K, Nariai Y, Yoshimura Y (2003) Carboplatin induces Fas (APO-1/CD95)-dependent apoptosis of human tongue carcinoma cells: sensitization for apoptosis by upregulation of FADD expression. Int J Cancer 105: 593-600. doi: 10.1002/ijc.11133
    [93] Woo SH, Park IC, Park MJ, et al. (2004) Arsenic trioxide sensitizes CD95/Fas-induced apoptosis through ROS-mediated upregulation of CD95/Fas by NF-kappaB activation. Int J Cancer 112: 596-606. doi: 10.1002/ijc.20433
    [94] Hallett WH, Ames E, Motarjemi M, et al. (2008) Sensitization of tumor cells to NK cell-mediated killing by proteasome inhibition. J Immunol 180: 163-170. doi: 10.4049/jimmunol.180.1.163
    [95] Symes JC, Kunin M, Fleshner NE, et al. (2008) Fas-mediated killing of primary prostate cancer cells is increased by mitoxantrone and docetaxel. Mol Cancer Ther 7: 3018-3028. doi: 10.1158/1535-7163.MCT-08-0335
    [96] Llobet D, Eritja N, Yeramian A, et al. (2010) The multikinase inhibitor sorafenib induces apoptosis and sensitizes endometrial cancer cells to TRAIL by different mechanisms. Eur J Cancer 46: 836-850. doi: 10.1016/j.ejca.2009.12.025
    [97] Zhang G, Park MA, Mitchell C, et al. (2008) Vorinostat and sorafenib synergistically kill tumor cells via FLIP suppression and CD95 activation. Clin Cancer Res 14: 5385-5399. doi: 10.1158/1078-0432.CCR-08-0469
    [98] Bonnotte B, Favre N, Reveneau S, et al. (1998) Cancer cell sensitization to Fas-mediated apoptosis by sodium butyrate. Cell Death Differ 5: 480-487. doi: 10.1038/sj.cdd.4400371
    [99] Rivkin I, Cohen K, Bod T, et al. (2014) Cancer cell sensitization and improved treatment efficacy by combined sodium butyrate and paclitaxel formulations is cancer-type specific. Int J Pharm 461: 437-447. doi: 10.1016/j.ijpharm.2013.12.021
    [100] Kondo G, Iwase M, Watanabe H, et al. (2006) Enhancement of susceptibility to Fas-mediated apoptosis in oral squamous cell carcinoma cells by phosphatidylinositol 3-kinase inhibitor. Oral Oncol 42: 745-752. doi: 10.1016/j.oraloncology.2005.11.015
    [101] Rao-Bindal K, Zhou Z, Kleinerman ES (2012) MS-275 sensitizes osteosarcoma cells to Fas ligand-induced cell death by increasing the localization of Fas in membrane lipid rafts. Cell Death Dis 3: e369. doi: 10.1038/cddis.2012.101
    [102] Castro BM, de Almeida RF, Goormaghtigh E, et al. (2011) Organization and dynamics of Fas transmembrane domain in raft membranes and modulation by ceramide. Biophys J 101: 1632-1641. doi: 10.1016/j.bpj.2011.08.022
    [103] Gajate C, Del Canto-Jañez E, Acuña AU, et al. (2004) Intracellular triggering of Fas aggregation and recruitment of apoptotic molecules into Fas-enriched rafts in selective tumor cell apoptosis. J Exp Med 200: 353-365. doi: 10.1084/jem.20040213
    [104] Mollinedo F, de la Iglesia-Vicente J, Gajate C, et al. (2010) In vitro and in vivo selective antitumor activity of Edelfosine against mantle cell lymphoma and chronic lymphocytic leukemia involving lipid rafts. Clin Cancer Res 16: 2046-2054. doi: 10.1158/1078-0432.CCR-09-2456
    [105] Rajesh D, Stenzel RA, Howard SP (2003) Perillyl alcohol as a radio-/chemosensitizer in malignant glioma. J Biol Chem 278: 35968-35978. doi: 10.1074/jbc.M303280200
    [106] Westerndorp MO, Frank R, Ochsenbauer C, et al. (1995) Sensitization of T cells to CD95-mediated apoptosis by HIV-1 Tat and gp120. Nature 375: 497-500. doi: 10.1038/375497a0
    [107] Ruggieri A, Harada T, Matsuura Y, et al. (1997) Sensitization to Fas-mediated apoptosis by hepatitis C virus core protein. Virology 229: 68-76. doi: 10.1006/viro.1996.8420
    [108] Tanaka M, Suda T, Yatomi T, et al. (1997) Lethal effect of recombinant human Fas ligand in mice pretreated with Propionibacterium acnesJ Immunol 158: 2303-2309.
    [109] Wagner S, Beil W, Westermann J, et al. (1997) Regulation of gastric epithelial cell growth by Helicobacter pylori: evidence for a major role of apoptosis. Gastroenterology 113: 1836-1847. doi: 10.1016/S0016-5085(97)70003-9
    [110] Chakraborty M, Abrams SI, Camphausen K, et al. (2003) Irradiation of tumor cells up-regulates Fas and enhances CTL lytic activity and CTL adoptive immunotherapy. J Immunol 170: 6338-6347. doi: 10.4049/jimmunol.170.12.6338
    [111] Park IC, Woo SH, Park MJ, et al. (2003) Ionizing radiation and nitric oxide donor sensitize Fas-induced apoptosis via up-regulation of Fas in human cervical cancer cells. Oncol Rep 10: 629-633.
    [112] Schroder K, Herztog PJ, Ravasi T, et al. (2004) Interferon-γ: an overview of signals, mechanisms and functions. J Leukoc Biol 75: 163-189. doi: 10.1189/jlb.0603252
    [113] Zaidi MR, Merlino G (2011) The two faces of interferon-γ in cancer. Clin Cancer Res 17: 6118-6124. doi: 10.1158/1078-0432.CCR-11-0482
    [114] Meissl K, Macho-Maschler S, Müller M, et al. (2015) The good and the bad faces of STAT1 in solid tumors. Cytokine 89: 12-20. doi: 10.1016/j.cyto.2015.11.011
    [115] Showalter A, Limaye A, Oyer JL, et al. (2017) Cytokines in immunogenic cell death: applications for cancer immunotherapy. Cytokine 97: 123-132. doi: 10.1016/j.cyto.2017.05.024
    [116] Burke JD, Young HA (2019) IFN-γ: a cytokine at the right time, is in the right place. Semin Immunol 43: 101280. doi: 10.1016/j.smim.2019.05.002
    [117] Yonehara S, Ishii A, Yonehara M (1989) A cell-killing monoclonal antibody (anti-Fas) to a cell surface antigen co-downregulated with the receptor of tumor necrosis factor. J Exp Med 169: 1747-1756. doi: 10.1084/jem.169.5.1747
    [118] Günthert AR, Sträter J, von Reyher U, et al. (1996) Early detachment of colon carcinoma cells during CD95 (APO-1/Fas)-mediated apoptosis. I. de-adhesion from hyaluronate by shedding of CD44. J Cell Biol 134: 1089-1096. doi: 10.1083/jcb.134.4.1089
    [119] Ossina NK, Cannas A, Powers VC, et al. (1997) Interferon-γ modulates a p53-independent apoptotic pathway and apoptosis-related gene expression. J Biol Chem 272: 16351-16357. doi: 10.1074/jbc.272.26.16351
    [120] Tillman DM, Harwood FG, Gibson AA, et al. (1998) Expression of genes that regulate Fas signaling and Fas-mediated apoptosis in colon carcinoma cells. Cell Death Differ 5: 450-457. doi: 10.1038/sj.cdd.4400369
    [121] Darcy PK, Kershaw MH, Trapani JA, et al. (1998) Expression in cytotoxic T lymphocytes of a single-chain anti-carcinoembryonic antigen antibody. Redirected Fas ligand-mediated lysis of colon carcinoma. Eur J Immunol 28: 1663-1672. doi: 10.1002/(SICI)1521-4141(199805)28:05<1663::AID-IMMU1663>3.0.CO;2-L
    [122] Koshiji M, Adachi Y, Sogo S, et al. (1998) Apoptosis of colorectal adenocarcinoma (COLO 201) by tumour necrosis factor (TNF-α) and/or interferon-gamma (IFN-γ), resulting from down-modulation of Bcl-2 expression. Clin Exp Immunol 111: 211-218. doi: 10.1046/j.1365-2249.1998.00460.x
    [123] von Reyher U, Sträter J, Kittstein W, et al. (1998) Colon carcinoma cells use different mechanisms to escape CD95-mediated apoptosis. Cancer Res 58: 526-534.
    [124] Xu X, Fu XY, Plate J, et al. (1998) IFN-γ induces cell growth inhibition by Fas-mediated apoptosis: requirement of STAT1 protein for up-regulation of Fas and FasL expression. Cancer Res 58: 2832-2837.
    [125] Rapoport E, Pendu JL (1999) Glycosylation alterations of cells in late phase apoptosis from colon carcinomas. Glycobiology 9: 1337-1345. doi: 10.1093/glycob/9.12.1337
    [126] Tillman DM, Petak I, Houghton JA (1999) A Fas-dependent component in 5-fluorouracil/leucovorin-induced cytotoxicity in colon carcinoma cells. Clin Cancer Res 5: 425-430.
    [127] Bergmann-Leitner ES, Abrams SI (2000) Influence of interferon γ on modulation of Fas expression by human colon carcinoma cells and their subsequent sensitivity to antigen-specific CD8+ cytotoxic T lymphocyte attack. Cancer Immunol Immunother 49: 193-207. doi: 10.1007/s002620000105
    [128] Bergmann-Leitner ES, Abrams SI (2000) Differential role of Fas/Fas ligand interactions in cytolysis of primary and metastatic colon carcinoma cell lines by human antigen-specific CD8+ CTL. J Immunol 164: 4941-4954. doi: 10.4049/jimmunol.164.9.4941
    [129] O'connell J, Bennett MW, Nally K, et al. (2000) Interferon-γ sensitizes colonic epithelial cell lines to physiological and therapeutic inducers of colonocyte apoptosis. J Cell Physiol 185: 331-338. doi: 10.1002/1097-4652(200012)185:3<331::AID-JCP3>3.0.CO;2-V
    [130] Remacle-Bonnet MM, Garrouste FL, Heller S, et al. (2000) Insulin-like growth factor-I protects colon cancer cells from death factor-induced apoptosis by potentiating tumor necrosis factor α-induced mitogen-activated protein kinase and nuclear factor κB signaling pathways. Cancer Res 60: 2007-2017.
    [131] Manos EJ, Jones DA (2001) Assessment of tumor necrosis factor receptor and Fas signaling pathways by transcriptional profiling. Cancer Res 61: 433-438.
    [132] Martin CA, Panja A (2002) Cytokine regulation of human intestinal primary epithelial cell susceptibility to Fas-mediated apoptosis. Am J Physiol Gastrointest Liver Physiol 282: G92-G104. doi: 10.1152/ajpgi.2002.282.1.G92
    [133] Schwartzberg LS, Petak I, Stewart C, et al. (2002) Modulation of Fas signaling pathway by IFN-γ in therapy of colon cancer: phase I trial and correlative studies of IFN-γ, 5-fluorouracil, and leucovorin. Clin Cancer Res 8: 2488-2498.
    [134] Wilson CA, Browning JL (2002) Death of HT29 adenocarcinoma cells induced by TNF family receptor activation is caspase-independent and displays features of both apoptosis and necrosis. Cell Death Differ 9: 1321-1333. doi: 10.1038/sj.cdd.4401107
    [135] Geller J, Petak I, Szucs KS, et al. (2003) Interferon-γ-induced sensitization of colon carcinomas to ZD9331 targets caspases, downstream of Fas, independent of mitochondrial signaling and the inhibitor of apoptosis survivin. Clin Cancer Res 9: 6504-6515.
    [136] Liu K, Abrams SI (2003) Coordinate regulation of IFN consensus sequence-binding protein and caspase-1 in the sensitization of human colon carcinoma cells to Fas-mediated apoptosis by IFN-γ. J Immunol 170: 6329-6337. doi: 10.4049/jimmunol.170.12.6329
    [137] Liu K, McDuffie E, Abrams SI (2003) Exposure of human primary colon carcinoma cells to anti-Fas interactions influences the emergence of pre-existing Fas-resistant metastatic subpopulations. J Immunol 171: 4164-4174. doi: 10.4049/jimmunol.171.8.4164
    [138] Seidelin JB, Jäättelä M, Nielsen OH (2004) Continuous interferon-γ or tumor necrosis factor-α exposure of enterocytes attenuates cell death responses. Cytokine 27: 113-119. doi: 10.1016/j.cyto.2004.04.001
    [139] Turner PK, Houghton JA, Petak I, et al. (2004) Interferon-gamma pharmacokinetics and pharmacodynamics in patients with colorectal cancer. Cancer Chemother Pharmacol 53: 253-260. doi: 10.1007/s00280-003-0723-8
    [140] Vekemans K, Braet F, Muyllaert D, et al. (2004) Nitric oxide from rat liver sinusoidal endothelial cells induces apoptosis in IFN γ-sensitized CC531s colon carcinoma cells. J Hepatol 41: 11-18. doi: 10.1016/j.jhep.2004.03.026
    [141] Siegmund D, Wicovsky A, Schmitz I (2005) Death receptor-induced signaling pathways are differentially regulated by gamma interferon upstream of caspase-8 processing. Mol Cell Biol 25: 6363-6379. doi: 10.1128/MCB.25.15.6363-6379.2005
    [142] Saha A, Chatterjee SK, Foon KA, et al. (2006) Anti-idiotype antibody induced cellular immunity in mice transgenic for human carcinoembryonic antigen. Immunology 118: 483-496.
    [143] Geng L, Zhu B, Dai BH, et al. (2011) A let-7/Fas double-negative feedback loop regulates human colon carcinoma cells sensitivity to Fas-related apoptosis. Biochem Biophys Res Comm 408: 494-499. doi: 10.1016/j.bbrc.2011.04.074
    [144] Shadrin N, Shapira MG, Khalfin B, et al. (2015) Serine protease inhibitors interact with IFN-γ through up-regulation of FasR; a novel therapeutic strategy against cancer. Exp Cell Res 330: 233-239. doi: 10.1016/j.yexcr.2014.11.005
    [145] Muraki M, Hirota K (2018) Confirmation of covalently-linked structure and cell-death inducing activity in site-specific chemical conjugates of human Fas ligand extracellular domain. BMC Res Notes 11: 395. doi: 10.1186/s13104-018-3501-8
    [146] Muraki M, Hirota K (2019) Site-specific biotin-group conjugate of human Fas ligand extracellular domain: preparation and characterization of cell-death-inducing activity. Curr Top Pep Prot Res 20: 17-24.
    [147] Morimoto H, Yonehara S, Bonavida B (1993) Overcoming tumor necrosis factor and drug resistance of human tumor cell lines by combination treatment with anti-Fas antibody and drugs or toxins. Cancer Res 53: 2591-2596.
    [148] Biswas P, Poli G, Orenstein JM, et al. (1994) Cytokine-mediated induction of human immunodeficiency virus (HIV) expression and cell death in chronically infected U1 cells: do tumor necrosis factor alpha and gamma interferon selectively kill HIV-infected cells? J Virol 68: 2598-2604. doi: 10.1128/JVI.68.4.2598-2604.1994
    [149] Shima Y, Nishimoto N, Ogata A, et al. (1995) Myeloma cells express Fas antigen/APO-1 (CD95) but only some are sensitive to anti-Fas antibody resulting in apoptosis. Blood 85: 757-764. doi: 10.1182/blood.V85.3.757.bloodjournal853757
    [150] Efferth T, Fabry U, Osieka R (1996) Anti-Fas/Apo-1 monoclonal antibody CH-11 depletes glutathione and kills multidrug-resistant human leukemic cells. Blood Cell Mol Dis 22: 2-9. doi: 10.1006/bcmd.1996.0002
    [151] Spets H, Georgii-Hemming P, Siljason J, et al. (1998) Fas/APO-1 (CD95)-mediated apoptosis is activated by interferon-γ and interferon-α in interleukin-6 (IL-6)-dependent and IL-6-independent multiple myeloma cell lines. Blood 92: 2914-2923. doi: 10.1182/blood.V92.8.2914
    [152] Horie T, Dobashi K, Iizuka K, et al. (1999) Interferon-γ rescues TNF-α-induced apoptosis mediated by up-regulation of TNFR2 on EoL-1 cells. Exp Hematol 27: 512-519. doi: 10.1016/S0301-472X(98)00058-7
    [153] Sata M, Suhara T, Walsh K (2000) Vascular endothelial cells and smooth muscle cells differ in expression of Fas and Fas ligand and in sensitivity to Fas ligand-induced cell death. Implications for vascular disease and therapy. Arterioscler Thromb Vasc Biol 20: 309-316. doi: 10.1161/01.ATV.20.2.309
    [154] Varela N, Muñoz-Pinedo C, Ruiz-Ruiz C, et al. (2001) Interferon-γ sensitizes human myeloid leukemia cells to death receptor-mediated apoptosis by a pleiotropic mechanism. J Biol Chem 276: 17779-17787. doi: 10.1074/jbc.M100815200
    [155] Dörrie J, Sapala K, Zunino SJ (2002) Interferon-γ increases the expression of glycosylated CD95 in B-leukemic cells: an inducible model to study the role of glycosylation in CD95-signalling and trafficking. Cytokine 18: 98-107. doi: 10.1006/cyto.2002.1030
    [156] Jedema I, Barge RMY, Willemze R, et al. (2003) High susceptibility of human leukemic cells to Fas-induced apoptosis is restricted to G1 phase of the cell cycle and can be increased by interferon treatment. Leukemia 17: 576-584. doi: 10.1038/sj.leu.2402844
    [157] Dimberg LY, Dimberg AI, Ivarsson K, et al. (2005) Ectopic and IFN-induced expression of Fas overcomes resistance to Fas-mediated apoptosis in multiple myeloma cells. Blood 106: 1346-1354. doi: 10.1182/blood-2004-04-1322
    [158] Guy CS, Wang J, Michalak TI (2006) Hepatocytes as cytotoxic effector cells can induce cell death by CD95 ligand-mediated pathway. Hepatology 43: 1231-1240. doi: 10.1002/hep.21201
    [159] Boselli D, Ragimbeau J, Orlando L, et al. (2010) Expression of IFNγR2 mutated in a dileucine internalization motif reinstates IFNγ signaling and apoptosis in human T lymphocytes. Immunol Lett 134: 17-25. doi: 10.1016/j.imlet.2010.08.005
    [160] Dimberg LY, Dimberg A, Ivarsson K, et al. (2012) Stat1 activation attenuates IL-6 induced Stat3 activity but does not alter apoptosis sensitivity in multiple myeloma. BMC Cancer 12: 318. doi: 10.1186/1471-2407-12-318
    [161] Fujihara Y, Takato T, Hoshi K (2014) Macrophage-inducing FasL on chondrocytes forms immune privilege in cartilage tissue engineering, enhancing in vivo regeneration. Stem Cell 32: 1208-1219. doi: 10.1002/stem.1636
    [162] Xia HL, Li CJ, Hou XF, et al. (2017) Interferon-γ affects leukemia cell apoptosis through regulating Fas/FasL signaling pathway. Eur Rev Med Pharmacol Sci 21: 2244-2248.
    [163] Weller M, Frei K, Groscurth P, et al. (1994) Anti-Fas/APO-1 antibody-mediated apoptosis of cultured human glioma cells. Induction and modulation of sensitivity by cytokines. J Clin Invest 94: 954-964. doi: 10.1172/JCI117462
    [164] Fulda S, Debatin KM (2002) IFNγ sensitizes for apoptosis by upregulating caspase-8 expression through the Stat1 pathway. Oncogene 21: 2295-2308. doi: 10.1038/sj.onc.1205255
    [165] Buntinx M, Gielen E, van Hummelen P, et al. (2004) Cytokine-induced cell death in human oligodendroglial cell lines. II: alterations in gene expression induced by interferon-γ and tumor necrosis factor-α. J Neurosci Res 76: 846-861. doi: 10.1002/jnr.20117
    [166] Choi C, Jeong E, Benveniste EN (2004) Caspase-1 mediates Fas-induced apoptosis and is up-regulated by interferon-γ in human astrocytoma cells. J Neuro-oncol 67: 167-176. doi: 10.1023/B:NEON.0000021896.52664.9e
    [167] Song JH, Wang CX, Song DK, et al. (2005) Interferon γ induces neurite outgrowth by up-regulation of p35 neuron-specific cycline-dependent kinase 5 activator via activation of ERK1/2 pathway. J Biol Chem 280: 12896-12901. doi: 10.1074/jbc.M412139200
    [168] Giammarioli AM, Vona R, Gambardella L, et al. (2009) Interferon-γ bolsters CD95/Fas-mediated apoptosis of astroglioma cells. FEBS J 276: 5920-5935. doi: 10.1111/j.1742-4658.2009.07271.x
    [169] Wen LP, Madani K, Fahrni JA, et al. (1997) Dexamethasone inhibits lung epithelial cell apoptosis induced by IFN-γ and Fas. Am J Physiol 273: L921-L929.
    [170] Maeyama T, Kuwano K, Kawasaki M, et al. (2001) Upregulation of Fas-signaling molecules in lung epithelial cells from patients with idiopathic pulmonary fibrosis. Eur Respir J 17: 180-189. doi: 10.1183/09031936.01.17201800
    [171] Coulter KR, Doseff A, Sweeney P, et al. (2002) Opposing effect by cytokines on Fas-mediated apoptosis in A549 lung epithelial cells. Am J Respir Cell Mol Biol 26: 58-66. doi: 10.1165/ajrcmb.26.1.4285
    [172] Kim KB, Choi YH, Kim IK, et al. (2002) Potentiation of Fas- and TRAIL-mediated apoptosis by IFN-γ in A549 lung epithelial cells: enhancement of caspase-8 expression through IFN-response element. Cytokine 20: 283-288. doi: 10.1006/cyto.2003.2008
    [173] Hopkins-Donaldson S, Ziegler A, Kurtz S, et al. (2003) Silencing of death receptor and caspase-8 expression in small cell lung carcinoma cell lines and tumours by DNA methylation. Cell Death Differ 10: 356-364. doi: 10.1038/sj.cdd.4401157
    [174] Crescenzi E, Pacifico F, Lavorgna A, et al. (2011) NF-κB-dependent cytokine secretion controls Fas expression on chemotherapy-induced premature senescent tumor cells. Oncogene 30: 2707-2717. doi: 10.1038/onc.2011.1
    [175] Keane MM, Ettenberg SA, Lowrey GA, et al. (1996) Fas expression and function in normal and malignant breast cell lines. Cancer Res 56: 4791-4798.
    [176] Haynes NM, Smyth MJ, Kershaw MH, et al. (1999) Fas-ligand-mediated lysis of erbB-2-expressing tumour cells by redirected cytotoxic T lymphocytes. Cancer Immunol Immunother 47: 278-286. doi: 10.1007/s002620050532
    [177] Danforth DN, Zhu Y (2005) Conversion of Fas-resistant to Fas-sensitive MCF-7 breast cancer cells by the synergistic interaction of interferon-γ and all-trans retinoic acid. Breast Cancer Res Treat 94: 81-91. doi: 10.1007/s10549-005-7491-6
    [178] Deiss LP, Galinka H, Beriss H, et al. (1996) Cathepsin D protease mediates programmed cell death induced by interferon-γ, Fas/APO-1 and TNF-α. EMBO J 15: 3861-3870. doi: 10.1002/j.1460-2075.1996.tb00760.x
    [179] Jauharoh SNA, Saegusa J, Sugimoto T, et al. (2012) SS-A/Ro52 promotes apoptosis by regulating Bcl-2 production. Biochem Biophys Res Comm 417: 582-587. doi: 10.1016/j.bbrc.2011.12.010
    [180] Boeddeker SJ, Baston-Buest DM, Altergot-Ahmad O, et al. (2014) Syndecan-1 knockdown in endometrial epithelial cells alters their apoptotic protein profile and enhances the inducibility of apoptosis. Mol Hum Reprod 20: 567-578. doi: 10.1093/molehr/gau009
    [181] Yang D, Thangaraju M, Browing DD, et al. (2007) IFN regulatory factor 8 mediates apoptosis in nonhemopoietic tumor cells via regulation of Fas expression. J Immunol 179: 4775-4782. doi: 10.4049/jimmunol.179.7.4775
    [182] Banik D, Khan ANH, Walseng E, et al. (2012) Interferon regulatory factor-8 is important for histone deacetylase inhibitor-mediated antitumor activity. Plos One 7: e45422. doi: 10.1371/journal.pone.0045422
    [183] Nonomura N, Miki T, Yokoyama M, et al. (1996) Fas/APO-1-mediated apoptosis of human renal cell carcinoma. Biochem Biophys Res Comm 229: 945-951. doi: 10.1006/bbrc.1996.1906
    [184] Lee JK, Sayers TJ, Brooks AD, et al. (2000) IFN-γ-dependent delay of in vivo tumor progression by Fas overexpression of murine renal cancer cells. J Immunol 164: 231-239. doi: 10.4049/jimmunol.164.1.231
    [185] Tomita Y, Bilim V, Hara N, et al. (2003) Role of IRF-1 and caspase-7 in IFN-γ enhancement of Fas-mediated apoptosis in ACHN renal cell carcinoma cells. Int J Cancer 104: 400-408. doi: 10.1002/ijc.10956
    [186] García-Sánchez O, López-Novoa JM, López-Hermández FJ (2014) Interferon-γ reduces the proliferation of primed human renal tubular cells. Nephron Extra 4: 1-7. doi: 10.1159/000353587
    [187] Ugurel S, Seiter S, Pappl G, et al. (1999) Heterogeneous susceptibility to CD95-induced apoptosis in melanoma cells correlates with bcl-2 and bcl-x expression and is sensitive to modulation by interferon-γ. Int J Cancer 82: 727-736. doi: 10.1002/(SICI)1097-0215(19990827)82:5<727::AID-IJC17>3.0.CO;2-E
    [188] Shchors K, Yehiely F, Deiss LP (2004) Cell death inhibiting RNA (CDIR) modulates IFN-γ-stimulated sensitization to Fas/CD95/Apo-1 and TRAIL/Apo2L-induced apoptosis. Cell Cycle 3: 1606-1611. doi: 10.4161/cc.3.12.1295
    [189] Hiramoto K, Inui M, Kamei T, et al. (2006) mHFE7A, a newly identified monoclonal antibody to Fas, induces apoptosis in human melanoma cells in vitro and delays the growth of melanoma xenotransplants. Oncol Rep 15: 409-415.
    [190] Fellenberg J, Mau H, Scheuerpflug C, et al. (1997) Modulation of resistance to anti-APO-1-induced apoptosis in osteosarcoma cells by cytokines. Int J Cancer 72: 536-542. doi: 10.1002/(SICI)1097-0215(19970729)72:3<536::AID-IJC25>3.0.CO;2-8
    [191] Li Z, Xu Q, Peng H, et al. (2011) IFN-γ enhances HOS and U2OS cell lines susceptibility to γδ T cell-mediated killing through the Fas/Fas ligand pathway. Int Immnonopharmacol 11: 496-503. doi: 10.1016/j.intimp.2011.01.001
    [192] Garbán HJ, Bonavida B (1999) Nitric oxide sensitizes ovarian tumor cells to Fas-induced apoptosis. Gynecol Oncol 73: 257-264. doi: 10.1006/gyno.1999.5374
    [193] Jones NL, Day AS, Jennings HA, et al. (1999) Helicobacter pylori induces gastric epithelial cell apoptosis in association with increased Fas receptor expression. Infect Immun 67: 4237-4242. doi: 10.1128/IAI.67.8.4237-4242.1999
    [194] Wang J, Fan X, Lindholm C, et al. (2000) Helicobacter pylori modulates lymphoepithelial cell interactions leading to epithelial cell damage through Fas/Fas ligand interactions. Infect Immun 68: 4303-4311. doi: 10.1128/IAI.68.7.4303-4311.2000
    [195] Shin EC, Shin WC, Choi Y, et al. (2001) Effect of interferon-γ on the susceptibility to Fas (CD95/APO-1)-mediated cell death in human hepatoma cells. Cancer Immunol Immunother 50: 23-30. doi: 10.1007/s002620000166
    [196] Ahn EY, Pan G, Vickers SM, et al. (2002) IFN-γ upregulates apoptosis-related molecules and enhances Fas-mediated apoptosis in human cholangiocarcinoma. Int J Cancer 100: 445-451. doi: 10.1002/ijc.10516
    [197] Tsuji S, Hosotani R, Yonehara S, et al. (2003) Endogenous decoy receptor 3 blocks the growth inhibition signals mediated by Fas ligand in human pancreatic adenocarcinoma. Int J Cancer 106: 17-25. doi: 10.1002/ijc.11170
    [198] Selleck WA, Canfield SE, Hassen WA, et al. (2003) IFN-γ sensitization of prostate cancer cells to Fas-mediated death: a gene therapy approach. Mol Ther 7: 185-192. doi: 10.1016/S1525-0016(02)00040-0
    [199] Amrani A, Verdaguer J, Thiessen S, et al. (2000) IL-1α, IL-1β, and IFN-γ mark β cells for Fas-dependent destruction by diabetogenic CD4+ T lymphocytes. J Clin Invest 105: 459-468. doi: 10.1172/JCI8185
    [200] Mollah ZUA, Wail J, McKenzie MD, et al. (2011) The pro-apoptotic BH3-only protein Bid is dispensable for development of insulitis and diabetes in the non-obese diabetic mouse. Apoptosis 16: 822-830. doi: 10.1007/s10495-011-0615-z
    [201] Augstein P, Bahr J, Wachlin G, et al. (2004) Cytokines activate caspase-3 in insulinoma cells of diabetes-prone NOD mice directly and via upregulation of Fas. J Autoimmun 23: 301-309. doi: 10.1016/j.jaut.2004.09.006
    [202] Igoillo-Esteve M, Gurzov EN, Eizirik DL, et al. (2011) The transcription factor B-cell lymphoma (BCL)-6 modulates pancreatic β-cell inflammatory responses. Endocrinology 152: 447-456. doi: 10.1210/en.2010-0790
    [203] Allagnat F, Fukaya M, Nogueira TC, et al. (2012) C/EBP homologous protein contributes to cytokine-induced pro-inflammatory responses and apoptosis in β-cells. Cell Death Differ 19: 1836-1846. doi: 10.1038/cdd.2012.67
    [204] Nardelli TR, Vanzela EC, Benedicto KC, et al. (2018) Prolactin protects against cytokine-induced beta-cell death by NFκB and JNK inhibition. J Mol Endocrinol 61: 25-36. doi: 10.1530/JME-16-0257
    [205] Kawakami A, Eguchi K, Matsuoka N, et al. (1997) Modulation of Fas-mediated apoptosis of human thyroid epithelial cells by IgG from patients with Graves' disease (GD) and idiopathic myxoedema. Clin Exp Immunol 110: 434-439. doi: 10.1046/j.1365-2249.1997.4301447.x
    [206] Stassi G, Di Liberto D, Todaro M, et al. (2000) Control of target cell survival in thyroid autoimmunity by T helper cytokines via regulation of apoptotic proteins. Nat Immunol 1: 483-488. doi: 10.1038/82725
    [207] Pouly S, Becher B, Blain M, et al. (2000) Interferon-γ modulates human oligodendrocyte susceptibility to Fas-mediated apoptosis. J Neuropathol Exp Neurol 59: 280-286. doi: 10.1093/jnen/59.4.280
    [208] Yao Y, Lu S, Li H, et al. (2012) Low doses of exogenous interferon-γ attenuated airway inflammation through enhancing Fas/FasL-induced CD4+ T cell apoptosis in a mouse asthma model. J Interferon Cytokine Res 32: 534-541. doi: 10.1089/jir.2012.0016
    [209] Hallam DM, Capps NL, Travelstead AL, et al. (2000) Evidence for an interferon-related inflammatory reaction in the trisomy 16 mouse brain leading to caspase-1-mediated neuronal apoptosis. J Neuroimmunol 110: 66-75. doi: 10.1016/S0165-5728(00)00289-7
    [210] Ping L, Ogawa N, Sugai S (2005) Novel role of CD40 in Fas-dependent apoptosis of cultured salivary epithelial cells from patients with Sjögren's syndrome. Arthritis Rheum 52: 573-581. doi: 10.1002/art.20789
    [211] Fischer-Posovszky P, Hebestreit H, Hofmann AK, et al. (2006) Role of CD95-mediated adipocyte loss in autoimmune lipodystrophy. J Clin Endocrinol Metab 91: 1129-1135. doi: 10.1210/jc.2005-0737
    [212] Contassot E, Kerl K, Roques S, et al. (2008) Resistance to FasL and tumor necrosis factor-related apoptosis-inducing ligand-mediated apoptosis in Sézary syndrome T-cells associated with impaired death receptor and FLICE-inhibitory protein expression. Blood 111: 4780-4787. doi: 10.1182/blood-2007-08-109074
    [213] Conceiҫão-Silva F, Hahne M, Schröter M, et al. (1998) The resolution of lesions induced by Leishmania major in mice requires a functional Fas (APO-1, CD95) pathway of cytotoxicity. Eur J Immunol 28: 237-245. doi: 10.1002/(SICI)1521-4141(199801)28:01<237::AID-IMMU237>3.0.CO;2-O
    [214] Chakour R, Guler R, Bugnon M, et al. (2003) Both the Fas ligand and inducible nitric oxide synthase are needed for control of parasite replication within lesions in mice infected with Leishmania major whereas the contribution of tumor necrosis factor is minimal. Infect Immun 71: 5287-5295. doi: 10.1128/IAI.71.9.5287-5295.2003
    [215] Rosner D, Stoneman V, Littlewood T, et al. (2006) Interferon-γ induces Fas trafficking and sensitization to apoptosis in vascular smooth muscle cells via a PI3K- and Akt-dependent mechanism. Am J Pathol 168: 2054-2063. doi: 10.2353/ajpath.2006.050473
    [216] Esser P, Heimann K, Abts H, et al. (1995) CD95 (Fas/APO-1) antibody-mediated apoptosis of human retinal pigment epithelial cells. Biochem Biophys Res Comm 213: 1026-1034. doi: 10.1006/bbrc.1995.2231
    [217] Yang Z, Gagarin D, St. Laurent III G, et al. (2009) Cardiovascular inflammation and lesion cell apoptosis. A novel connection via the interferon-inducible immunoproteasome. Arterioscler Thromb Vasc Biol 29: 1213-1219. doi: 10.1161/ATVBAHA.109.189407
    [218] Zhaorigetu S, Yang Z, Toma I, et al. (2011) Apolipoprotein L6, induced in atherosclerotic lesions promotes apoptosis and blocks Beclin 1-dependent autophagy in atherosclerotic cells. J Biol Chem 286: 27389-27398. doi: 10.1074/jbc.M110.210245
    [219] Catalan MP, Subirá D, Reyero A, et al. (2003) Regulation of apoptosis by lethal cytokines in human mesothelial cells. Kidney Int 64: 321-330. doi: 10.1046/j.1523-1755.2003.00062.x
    [220] Wang XY, Crowston JG, Zoellner H, et al. (2007) Interferon-α and interferon-γ sensitize human tenon fibroblasts to mitomycin-C. Invest Ophthalmol Vis Sci 48: 3655-3661. doi: 10.1167/iovs.06-1121
    [221] Zhang X, Chen W, De Paiva CS, et al. (2011) Interferon-γ exacerbates dry eye-induced apoptosis in conjunctiva through dual apoptotic pathways. Invest Ophthalmol Vis Sci 52: 6279-6285. doi: 10.1167/iovs.10-7081
    [222] Nagafuji K, Shibuya T, Harada M, et al. (1995) Functional expression of Fas antigen (CD95) on hematopoietic progenitor cells. Blood 86: 883-889. doi: 10.1182/blood.V86.3.883.883
    [223] Oyaizu N, Mc Closkey TW, Than S, et al. (1996) Inhibition of CD4 cross-linking-induced lymphocytes apoptosis by vesnarinone as a novel immunomodulating agent: vesnarinone inhibits Fas expression and apoptosis by blocking cytokine secretion. Blood 87: 2361-2368. doi: 10.1182/blood.V87.6.2361.bloodjournal8762361
    [224] Sato T, Selleri C, Anderson S, et al. (1997) Expression and modulation of cellular receptors for interferon-γ, tumour necrosis factor, and Fas on human bone marrow CD34+ cells. Br J Haematol 97: 356-365. doi: 10.1046/j.1365-2141.1997.562704.x
    [225] Schneider E, Moreau G, Arnould A, et al. (1999) Increased fatal and extramedullary hematopoiesis in Fas-deficient C57BL/6-lpr/lpr mice. Blood 94: 2613-2621. doi: 10.1182/blood.V94.8.2613.420k33_2613_2621
    [226] Erie AJ, Samsel L, Takaku T, et al. (2011) MHC class II upregulation and colocalization with Fas in experimental models of immune-mediated bone marrow failure. Exp Hematol 39: 837-849. doi: 10.1016/j.exphem.2011.05.005
    [227] Kohara H, Kitaura H, Fujimura Y, et al. (2011) IFN-γ directly inhibits TNF-α-induced osteoclastgenesis in vitro and in vivo and induces apoptosis mediated by Fas/Fas ligand interactions. Immunol Lett 137: 53-61. doi: 10.1016/j.imlet.2011.02.017
    [228] Liu Y, Wang L, Kikuiri T, et al. (2011) Mesenchymal stem cell-based tissue regeneration is governed by recipient T lymphocytes via IFN-γ and TNF-α. Nat Med 17: 1594-1601. doi: 10.1038/nm.2542
    [229] Chen J, Feng X, Desierto MJ, et al. (2015) IFN-γ-mediated hematopoietic cell destruction in murine models of immune-mediated bone marrow failure. Blood 126: 2621-2631. doi: 10.1182/blood-2015-06-652453
    [230] Xu J, Wang Y, Li J, et al. (2016) IL-12p40 impairs mesenchymal stem cell-mediated bone regeneration via CD4+ T cells. Cell Death Differ 23: 1941-1951. doi: 10.1038/cdd.2016.72
    [231] Li X, Shang B, Li YN (2019) IFNγ and TNFα synergistically induce apoptosis of mesenchymal stem/stromal cells via induction of nitric oxide. Stem Cell Res Ther. 10: 18. doi: 10.1186/s13287-018-1102-z
    [232] Luttmann W, Opfer A, Dauer E, et al. (1998) Differential regulation of CD95 (Fas/APO-1) expression in human blood eosinophils. Eur J Immunol 28: 2057-2065. doi: 10.1002/(SICI)1521-4141(199807)28:07<2057::AID-IMMU2057>3.0.CO;2-T
    [233] Luttmann W, Dauer E, Schmidt S, et al. (2000) Effects of interferon-γ and tumour necrosis factor-α on CD95/Fas ligand-mediated apoptosis in human blood eosinophils. Scand J Immunol 51: 54-59. doi: 10.1046/j.1365-3083.2000.00645.x
    [234] Zizzo G, Cohen PL (2013) IL-17 stimulates differentiation of human anti-inflammatory macrophages and phagocytosis of apoptotic neutrophils in response to IL-10 and glucocorticoids. J Immunol 190: 5237-5246. doi: 10.4049/jimmunol.1203017
    [235] Hagmann BR, Odermatt A, Kaufmann T, et al. (2016) Balance between IL-3 and type I interferons and their interrelationship with FasL dictates lifespan and effector functions of human basophils. Clin Exp Allergy 47: 71-84. doi: 10.1111/cea.12850
    [236] Chung IJ, Dai C, Krantz SB (2003) Stem cell factor increases the expression of FLIP that inhibits IFN-γ-induced apoptosis in human erythroid progenitor cells. Blood 101: 1324-1328. doi: 10.1182/blood-2002-06-1720
    [237] Müschen M, Warskulat U, Peters-Regehr T, et al. (1999) Involvement of CD95 (Apo-1/Fas) ligand expressed by rat Kupffer cells in hepatic immunoregulation. Gastroenterology 116: 666-677. doi: 10.1016/S0016-5085(99)70189-7
    [238] Bárcena A, Park SW, Banapour B, et al. (1996) Expression of Fas/CD95 and Bcl-2 by primitive hematopoietic progenitors freshly isolated from human fetal liver. Blood 88: 2013-2025. doi: 10.1182/blood.V88.6.2013.bloodjournal8862013
    [239] Oh JE, Shim KY, Lee JI, et al. (2017) 1-Methyl-L-tryptophan promotes the apoptosis of hepatic stellate cells arrested by interferon-γ by increasing the expression of IFN-γRβ, IRF-1 and Fas. Int J Mol Med 40: 576-582. doi: 10.3892/ijmm.2017.3043
    [240] He W, Yang C, Xia L, et al. (2014) CD4+ T cells from food allergy model are resistant to TCR-dependent apoptotic induction. Cytokine 68: 32-39. doi: 10.1016/j.cyto.2014.03.010
    [241] Lightfoot YL, Chen J, Mathews CE (2011) Role of the mitochondria in immune-mediated apoptotic death of the human pancreatic β cell line βLox5. Plos One 6: e20617. doi: 10.1371/journal.pone.0020617
    [242] Sun Q, Xiang RL, Yang YL, et al. (2013) Suppressor of cytokine signaling 1 protects rat pancreatic islets from cytokine-induced apoptosis through Janus kinase/signal transducers and activators of transcription pathway. Chin Med J 126: 4048-4053.
    [243] Quirk SM, Cowan RG, Huber SH (1997) Fas antigen-mediated apoptosis of ovarian surface epithelial cells. Endocrinology 138: 4558-4566. doi: 10.1210/endo.138.11.5508
    [244] Taniguchi H, Yokomizo Y, Okuda K (2002) Fas-Fas ligand system mediates luteal cell death in bovine corpus luteum. Biol Reprod 66: 754-759. doi: 10.1095/biolreprod66.3.754
    [245] Galvao AM, Ramilo DW, Skarzynski DJ, et al. (2010) Is Fas/Fas ligand system involved in equine corpus luteum functional regression? Biol Reprod 83: 901-908. doi: 10.1095/biolreprod.110.084699
    [246] Hojo T, Al-zi'abi O, Komiyama J, et al. (2010) Expression and localization of FLIP, an anti-apoptotic factor, in the bovine corpus luteum. J Reprod Dev 56: 230-235. doi: 10.1262/jrd.09-185S
    [247] Woclawek-Potocka I, Kowalczyk-Zieba I, Tylingo M, et al. (2013) Effects of lysophosphatidic acid on tumor necrosis factor α and interferon γ action in the bovine corpus luteum. Mol Cell Endrocrinol 377: 103-111. doi: 10.1016/j.mce.2013.07.005
    [248] Quirk SM, Porter DA, Huber SC, et al. (1998) Potentiation of Fas-mediated apoptosis of murine granulosa cells by interferon-γ, tumor necrosis factor-α, and cycloheximide. Endocrinology 139: 4860-4869. doi: 10.1210/endo.139.12.6353
    [249] Lee HJ, Kim JY, Park JE, et al. (2016) Induction of Fas-mediated apoptosis by interferon-γ is dependent on granulosa cell differentiation and follicular maturation in the rat ovary. Dev Reprod 20: 315-329. doi: 10.12717/DR.2016.20.4.315
    [250] Aschkenazi S, Straszewski S, Verwer KMA, et al. (2002) Differential regulation and function of the Fas/Fas ligand system in human trophoblast cells. Biol Reprod 66: 1853-1861. doi: 10.1095/biolreprod66.6.1853
    [251] Balkundi DR, Ziegler JA, Watchko JF, et al. (2003) Regulation of FasL/Fas in human trophoblasts: possible implications for chorioamnionitis. Biol Reprod 69: 718-724. doi: 10.1095/biolreprod.102.013102
    [252] Riccioli A, Starace D, D'Alessio A, et al. (2000) TNF-α and IFN-γ regulate expression and function of the Fas system in the seminiferous epithelium. J Immunol 165: 743-749. doi: 10.4049/jimmunol.165.2.743
    [253] González-Cuadrado S, López-Armada MJ, Gómez-Guerrero C, et al. (1996) Anti-Fas antibodies induce cytolysis and apoptosis in cultured human mesangial cells. Kidney Int 49: 1064-1070. doi: 10.1038/ki.1996.155
    [254] Tsukinoki T, Sugiyama H, Sunami R, et al. (2004) Mesangial cell Fas ligand: upregulation in human lupus nephritis and NF-κB-mediated expression in cultured human mesangial cells. Clin Exp Nephrol 8: 196-205. doi: 10.1007/s10157-004-0301-3
    [255] Lorz C, Ortiz A, Justo P, et al. (2000) Proapoptotic Fas ligand is expressed by normal kidney tubular epithelium and injured glomeruli. J Am Soc Nephrol 11: 1266-1277.
    [256] Spanaus KS, Schlapbach R, Fontana A (1998) TNF-α and INF-γ render microglia sensitive to Fas ligand-induced apoptosis by induction of Fas expression and down-regulation of Bcl-2 and Bcl-xL. Eur J Immunol 28: 4398-4408. doi: 10.1002/(SICI)1521-4141(199812)28:12<4398::AID-IMMU4398>3.0.CO;2-Y
    [257] Schlapbach R, Spanaus KS, Malipiero U, et al. (2000) TGF-β induces the expression of the FLICE-inhibitory protein and inhibits Fas-mediated apoptosis of microglia. Eur J Immunol 30: 3680-3688. doi: 10.1002/1521-4141(200012)30:12<3680::AID-IMMU3680>3.0.CO;2-L
    [258] Falsig J, Latta M, Leist M (2004) Defined inflammatory states in astrocyte cultures: correlation with susceptibility towards CD95-driven apoptosis. J Neurochem 88: 181-193. doi: 10.1111/j.1471-4159.2004.02144.x
    [259] Coque E, Salsac C, Espinosa-Carrasco G, et al. (2019) Cytotoxic CD8+ T lymphocytes expressing ALS-causing SOD1 mutant selectively trigger death of spinal motoneurons. Proc Natl Acad Sci USA 116: 2312-2317. doi: 10.1073/pnas.1815961116
    [260] Sayama K, Yonehara S, Watanabe Y, et al. (1994) Expression of Fas antigen on keratinocytes in vivo and induction of apoptosis in cultured keratinocytes. J Invest Dermatol 103: 330-334. doi: 10.1111/1523-1747.ep12394858
    [261] Viard-Leveugle I, Gaide O, Jankovic D, et al. (2013) TNF-α and IFN-γ are potential inducers of Fas-mediated keratinocyte apoptosis through activation of inducible nitric oxide synthase in toxic epidermal necrolysis. J Invest Dermatol 133: 489-498. doi: 10.1038/jid.2012.330
    [262] Gao Z, Jin YQ, Wu W (2017) SOCS3 treatment prevents the development of alopecia areata by inhibiting CD8+ T cell-mediated autoimmune destruction. Oncotarget 8: 33432-33443. doi: 10.18632/oncotarget.16504
    [263] Li JH, Kluger MS, Madge LA, et al. (2002) Interferon-γ augments CD95 (APO-1/Fas) and pro-caspase-8 expression and sensitizes human vascular endothelial cells to CD95-mediated apoptosis. Am J Pathol 161: 1485-1495. doi: 10.1016/S0002-9440(10)64424-0
    [264] Yamaoka-Tojo M, Yamaguchi S, Nitobe J, et al. (2003) Dual response to Fas ligation in human endothelial cells: apoptosis and induction of chemokines, interleukin-8 and monocyte chemoattractant protein-1. Coron Artery Dis 14: 89-94. doi: 10.1097/00019501-200302000-00010
    [265] Shigeta A, Tada Y, Wang JY, et al. (2012) CD40 amplifies Fas-mediated apoptosis: a mechanism contributing to emphysema. Am J Physiol Lung Cell Mol Physiol 303: L141-L151. doi: 10.1152/ajplung.00337.2011
    [266] Kawakami A, Eguchi K, Matsuoka N, et al. (1996) Thyroid-stimulating hormone inhibits Fas antigen mediated apoptosis of human thyrocytes in vitroEndocrinology 137: 3163-3169. doi: 10.1210/endo.137.8.8754734
    [267] Mezosi E, Yamazaki H, Bretz JD, et al. (2002) Aberrant apoptosis in thyroid epithelial cells from goiter nodules. J Clin Endocrinol Metab 87: 4264-4272. doi: 10.1210/jc.2002-020111
    [268] Mezosi E, Wang SH, Utsugi S, et al. (2005) Induction and regulation of Fas-mediated apoptosis in human thyroid epithelial cells. Mol Endocrinol 19: 804-811. doi: 10.1210/me.2004-0286
    [269] Wang SH, van Antwerp M, Kuick R, et al. (2007) Microarray analysis of cytokine activation of apoptosis pathways in the thyroid. Endocrinology 148: 4844-4852. doi: 10.1210/en.2007-0126
    [270] Fang Y, Braley-Mullen H (2008) Cultured murine thyroid epithelial cells expressing transgenic Fas-associated death-like interleukin-1β converting enzyme inhibitory protein are protected from Fas-mediated apoptosis. Endocrinology 149: 3321-3329. doi: 10.1210/en.2008-0080
    [271] Marsumura R, Umemiya K, Goto T, et al. (2000) Interferon gamma and tumor necrosis factor alpha induce Fas expression and anti-Fas mediated apoptosis in a salivary ductal cell line. Clin Exp Rheumatol 18: 311-318.
    [272] Abu-Helu RF, Dimitriou ID, Kapsogeorgou EK, et al. (2001) Induction of salivary gland epithelial cell injury in Sjogren's syndrome: in vitro assessment of T cell-derived cytokines and Fas protein expression. J Autoimmun 17: 141-153. doi: 10.1006/jaut.2001.0524
    [273] Ruemmele FM, Russo P, Beaulieu JF, et al. (1999) Susceptibility to Fas-induced apoptosis in human nontumoral enterocytes: role of costimulatory factors. J Cell Physiol 181: 45-54. doi: 10.1002/(SICI)1097-4652(199910)181:1<45::AID-JCP5>3.0.CO;2-Q
    [274] Bharhani MS, Borojevic R, Basak S, et al. (2006) IL-10 protects mouse intestinal epithelial cells from Fas-induced apoptosis via modulating Fas expression and altering caspase-8 and FLIP expression. Am J Physiol Gastrointest Liver Physiol 291: G820-G829. doi: 10.1152/ajpgi.00438.2005
    [275] De Saint Jean M, Debbasch C, Rahmani M, et al. (2000) Fas-and interferon γ-induced apoptosis in Chang conjunctival cells: further investigations. Invest Ophthalomol Vis Sci 41: 2531-2543.
    [276] Gao J, Sana R, Calder V, et al. (2013) Mitochondrial permeability transition pore in inflammatory apoptosis of human conjunctival epithelial cells and T cells: effect of cyclosporine A. Invest Ophthalmol Vis Sci 54: 4717-4733. doi: 10.1167/iovs.13-11681
    [277] Nakamura M, Matute-Bello G, Liles WC, et al. (2004) Differential response of human lung epithelial cells to Fas-induced apoptosis. Am J Pathol 164: 1949-1958. doi: 10.1016/S0002-9440(10)63755-8
    [278] Arai M, Yoshioka S, Nishimura R, et al. (2014) Fas/FasL-mediated cell death in the bovine endometrium. Anim Reprod Sci. 151: 97-104. doi: 10.1016/j.anireprosci.2014.10.004
    [279] Frankel SK, Cosgrove GP, Cha SI, et al. (2006) TNF-α sensitizes normal and fibrotic human lung fibroblasts to Fas-induced apoptosis. Am J Respir Cell Mol Biol 34: 293-304. doi: 10.1165/rcmb.2005-0155OC
    [280] Lee JW, Oh JE, Rhee KJ, et al. (2019) Co-treatment with interferon-γ and 1-methyl tryptophan ameliorates cardiac fibrosis through cardiac myofibroblasts apoptosis. Mol Cell Biochem 458: 197-205. doi: 10.1007/s11010-019-03542-7
    [281] Fluhr H, Krenzer S, Stein GM, et al. (2007) Interferon-γ and tumor necrosis factor-α sensitize primarily resistant human endometrial stromal cells to Fas-mediated apoptosis. J Cell Sci 120: 4126-4133. doi: 10.1242/jcs.009761
    [282] Boeddeker SJ, Baston-Buest DM, Fehm T, et al. (2015) Decidualization and syndecan-1 knock down sensitize endometrial stromal cells to apoptosis induced by embryonic stimuli. Plos One 10: e0121103. doi: 10.1371/journal.pone.0121103
    [283] Yamada K, Takane-Gyotoku N, Yuan X, et al. (1996) Mouse islet cell lysis mediated by interleukin-1-induced Fas. Diabetologia 39: 1306-1312. doi: 10.1007/s001250050574
    [284] Roth W, Wagenknecht B, Dichgans J, et al. (1998) Interferon-α enhances CD95L-induced apoptosis of human malignant glioma cells. J Neuroimmunol 87: 121-129. doi: 10.1016/S0165-5728(98)00079-4
    [285] Dey BR, Yang YG, Szot GL, et al. (1998) Interleukin-12 inhibits Graft-Versus-Host disease through a Fas-mediated mechanism associated with alterations in donor T-cell activation and expansion. Blood 91: 3315-3322. doi: 10.1182/blood.V91.9.3315
    [286] Kobayashi T, Okamoto K, Kobata T, et al. (1999) Tumor necrosis factor α regulation of the Fas-mediated apoptosis-signaling pathway in synovial cells. Arthritis Rheum 42: 519-526. doi: 10.1002/1529-0131(199904)42:3<519::AID-ANR17>3.0.CO;2-Q
    [287] Houghton J, Macera-Bloch LS, Harrison L, et al. (2000) Tumor necrosis factor alpha and interleukin 1β up-regulate gastric mucosal Fas antigen expression in Helicobacter pylori infection. Infect Immun 68: 1189-1195. doi: 10.1128/IAI.68.3.1189-1195.2000
    [288] Kimura K, Gelmann EP (2000) Tumor necrosis factor-α and Fas activate complementary Fas-associated death domain-dependent pathways that enhance apoptosis induced by γ-irradiation. J Biol Chem 275: 8610-8617. doi: 10.1074/jbc.275.12.8610
    [289] Reddy P, Teshima T, Kukuruga M, et al. (2001) Interleukin-18 regulates acute graft-versus-host disease by enhancing Fas-mediated donor T cell apoptosis. J Exp Med 10: 1433-1440. doi: 10.1084/jem.194.10.1433
    [290] Elzey BD, Griffith TS, Herndon JM, et al. (2001) Regulation of Fas ligand-induced apoptosis by TNF. J Immunol 167: 3049-3056. doi: 10.4049/jimmunol.167.6.3049
    [291] Sharief MK, Semra YK (2002) Down-regulation of survivin expression in T lymphocytes after interferon beta-1a treatment in patients with multiple sclerosis. Arch Neurol 59: 1115-1121. doi: 10.1001/archneur.59.7.1115
    [292] Park SM, Park HY, Lee TH (2003) Functional effects of TNF-α on a human follicular dendritic cell line: persistent NF-κB activation and sensitization for Fas-mediated apoptosis. J Immunol 171: 3955-3962. doi: 10.4049/jimmunol.171.8.3955
    [293] Schlosser SF, Schuler M, Christoph PB, et al. (2003) Ribavirin and alpha interferon enhance death receptor-mediated apoptosis and caspase activation in human hepatoma cells. Antimicrob Agents Chemother 47: 1912-1921. doi: 10.1128/AAC.47.6.1912-1921.2003
    [294] Schneider E, Tonanny MB, Lisbonne M, et al. (2004) Pro-Th1 cytokines promote Fas-dependent apoptosis of immature peripheral basophils. J Immnunol 172: 5262-5268. doi: 10.4049/jimmunol.172.9.5262
    [295] Dondi E, Roué G, Yuste VJ (2004) A dual role of IFN-α in the balance between proliferation and death of human CD4+ T lymphocytes during primary response. J Immunol 173: 3740-3747. doi: 10.4049/jimmunol.173.6.3740
    [296] Kelly JD, Dai J, Eschwege P, et al. (2004) Downregulation of Bcl-2 sensitizes interferon-resistant renal cancer cells to Fas. Br J Cancer 91: 164-170. doi: 10.1038/sj.bjc.6601895
    [297] Wu X, Pan G, McKenna MA, et al. (2005) RANKL regulates Fas expression and Fas-mediated apoptosis in osteoclasts. J Bone Mineral Res 20: 107-116. doi: 10.1359/JBMR.041022
    [298] Park SM, Kim S, Choi JS, et al. (2005) TGF-β inhibits Fas-mediated apoptosis of a follicular dendritic cell line by down-regulating the expression of Fas and caspase-8: counteracting role of TGF-β on TNF sensitization of Fas-mediated apoptosis. J Immunol 174: 6169-6175. doi: 10.4049/jimmunol.174.10.6169
    [299] Drynda A, Quax PHA, Neumann M, et al. (2005) Gene transfer of tissue inhibitor of metalloproteinases-3 reverses the inhibitory effects of TNF-α on Fas-induced apoptosis in rheumatoid arthritis synovial fibroblasts. J Immunol 174: 6524-6531. doi: 10.4049/jimmunol.174.10.6524
    [300] Lindkvist A, Ivarsson K, Jernberg-Wiklund H, et al. (2006) Interferon-induced sensitization to apoptosis is associated with repressed transcriptional activity of the hTERT promoter in multiple myeloma. Biochem Biophys Res Comm 341: 1141-1148. doi: 10.1016/j.bbrc.2006.01.068
    [301] Huerta-Yepez S, Vega M, Garban H, et al. (2006) Involvement of the TNF-α autocrine-paracrine loop, via NF-κB and YY1, in the regulation of tumor cell resistance to Fas-induced apoptosis. Clin Immunol 120: 297-309. doi: 10.1016/j.clim.2006.03.015
    [302] Corazza N, Jakob S, Schaer C, et al. (2006) TRAIL receptor-mediated JNK activation and Bim phosphorylation critically regulate Fas-mediated liver damage and lethality. J Clin Invest 116: 2493-2499. doi: 10.1172/JCI27726
    [303] Yang J, Epling-Burnette PK, Painter JS, et al. (2008) Antigen activation and impaired Fas-induced death-inducing signaling complex formation in T-large-granular lymphocyte leukemia. Blood 111: 1610-1616. doi: 10.1182/blood-2007-06-093823
    [304] Nihal M, Ahsan H, Siddiqui IA, et al. (2009) (-)-Epigallocatechin-3-gallate (EGCG) sensitizes melanoma cells to interferon induced growth inhibition in a mouse model of human melanoma. Cell Cycle 8: 2057-2063. doi: 10.4161/cc.8.13.8862
    [305] Wu J, Wood GS (2011) Reduction of Fas/CD95 promoter methylation, upregulation of Fas protein, and enhancement of sensitivity to apoptosis in cutaneous T-cell lymphoma. Arch Dermatol 147: 443-449. doi: 10.1001/archdermatol.2010.376
    [306] Schmich K, Schlatter R, Corazza N, et al. (2011) Tumor necrosis factor α sensitizes primary murine hepatocytes to Fas/CD95-induced apoptosis in a Bim- and Bid-dependent manner. Hepatology 53: 282-292. doi: 10.1002/hep.23987
    [307] Roos WP, Jöst E, Belohlavek C, et al. (2011) Intrinsic anticancer drug resistance of malignant melanoma cells is abrogated by IFN-β and valproic acid. Cancer Res 71: 4150-4160. doi: 10.1158/0008-5472.CAN-10-3498
    [308] Fraietta JA, Mueller YM, Yang G, et al. (2013) Type I interferon upregulates Bak and contributes to T cell loss during human immunodeficiency virus (HIV) infection. Plos Pathog 9: e1003658. doi: 10.1371/journal.ppat.1003658
    [309] Lutz A, Sanwald J, Thomas M, et al. (2014) Interleukin-1β enhances FasL-induced caspase-3/-7 activity without increasing apoptosis in primary mouse hepatocytes. Plos One 9: e115603. doi: 10.1371/journal.pone.0115603
    [310] Faletti L, Peintner L, Neumann S, et al. (2018) TNFα sensitizes hepatocytes to FasL-induced apoptosis by NFκB-mediated Fas upregulation. Cell Death Dis 9: 909. doi: 10.1038/s41419-018-0935-9
    [311] Aggarwal BB, Gupta SC, Kim JH (2012) Historical perspectives on tumor necrosis factor and its superfamily: 25 years later, a golden journey. Blood 119: 651-655. doi: 10.1182/blood-2011-04-325225
    [312] van Boxel-Dezaire AHH, Rani MRS, Stark GR (2006) Complex modulation of cell type-specific signaling in response to type I interferons. Immunity 25: 361-372. doi: 10.1016/j.immuni.2006.08.014
    [313] Hunter CA, Timans J, Pisacane P, et al. (1997) Comparison of the effects of interleukin-1α, interleukin-1β and interferon-γ-inducing factor on the production of interferon-γ by natural killer. Eur J Immunol 27: 2787-2792. doi: 10.1002/eji.1830271107
    [314] Bonta IL, Ben-Efraim S (1993) Involvement of inflammatory mediators in macrophage antitumor activity. J Leukoc Biol 54: 613-626. doi: 10.1002/jlb.54.6.613
    [315] Stylianou E, Saklatvala J (1998) Interleukin-1. Int J Biochem Cell Biol 30: 1075-1079. doi: 10.1016/S1357-2725(98)00081-8
    [316] Miwa K, Asano M, Horai R, et al. (1998) Caspase 1-indenendent IL-1β release and inflammation induced by the apoptosis inducer Fas ligand. Nat Med 4: 1287-1292. doi: 10.1038/3276
    [317] Linkermann A, Qian J, Lettau M, et al. (2005) Considering Fas ligand as a target for therapy. Expert Opin Ther Targets 9: 119-134. doi: 10.1517/14728222.9.1.119
    [318] Villa-Morales M, Fernández-Piqueras (2012) Targeting the Fas/FasL signaling pathway in cancer therapy. Expert Opin Ther Targets 16: 85-101. doi: 10.1517/14728222.2011.628937
    [319] Michael-Robinson JM, Pandeya N, Cummings MC, et al. (2003) Fas ligand and tumour counter-attack in colorectal cancer stratified according to microsatellite instability status. J Pathol 201: 46-54. doi: 10.1002/path.1406
    [320] Ogasawara J, Watanabe-Fukunaga R, Adachi M, et al. (1993) Lethal effect of the anti-Fas antibody in mice. Nature 26: 806-809. doi: 10.1038/364806a0
    [321] Tsujimoto Y, Shimizu S (2000) Bcl-2 family: life-or-death switch. FEBS Lett 466: 6-10. doi: 10.1016/S0014-5793(99)01761-5
    [322] Zhuang S, Dermirs JT, Kochevar IE (2001) Protein kinase C inhibits singlet oxygen-induced apoptosis by decreasing caspase-8 activation. Oncogene 20: 6764-6776. doi: 10.1038/sj.onc.1204867
    [323] Suzuki Y, Ono Y, Hirabayashi Y (1998) Rapid and specific reactive oxygene species generation during Fas-mediated apoptosis. FEBS Lett 425: 209-212. doi: 10.1016/S0014-5793(98)00228-2
    [324] Reinehr R, Becker S, Eberle A, et al. (2005) Involvement of NADPH oxidase isoforms and Src family kinases in CD95-dependent hepatocyte apoptosis. J Biol Chem 280: 27179-27194. doi: 10.1074/jbc.M414361200
    [325] Selleri C, Sato T, Raiola AM, et al. (1997) Induction of nitric oxide synthase is involved in the mechanism of Fas-mediated apoptosis in heamopoietic cells. Br J Heamatol 99: 481-489. doi: 10.1046/j.1365-2141.1996.4323240.x
    [326] Solano-Gálvez SG, Abadi-Chiriti J, Gutiérrez-Velez L, et al. (2018) Apoptosis: activation and inhibition in health and disease. Med Sci 6: 54.
    [327] Seyrek K, Lavik IN (2019) Modulation of CD95-mediated signaling by post-translational modifications: towards understanding CD95 signaling networks. Apoptosis 24: 385-394. doi: 10.1007/s10495-019-01540-0
    [328] Pitti RM, Marsters SA, Lawrence DA, et al. (1998) Genomic amplification of a decoy receptor for Fas ligand in lung and colon cancer. Nature 396: 699-703. doi: 10.1038/25387
    [329] Liu W, Ramagopal U, Cheng H, et al. (2016) Crystal structure of the complex of human FasL and its decoy receptor DcR3. Structure 24: 2016-2023. doi: 10.1016/j.str.2016.09.009
  • This article has been cited by:

    1. Ariane Verdy, Priyanga Amarasekare, Alternative stable states in communities with intraguild predation, 2010, 262, 00225193, 116, 10.1016/j.jtbi.2009.09.011
    2. Vardit Makler-Pick, Matthew R. Hipsey, Tamar Zohary, Yohay Carmel, Gideon Gal, Intraguild Predation Dynamics in a Lake Ecosystem Based on a Coupled Hydrodynamic-Ecological Model: The Example of Lake Kinneret (Israel), 2017, 6, 2079-7737, 22, 10.3390/biology6020022
    3. Yuanshi Wang, Hong Wu, Shikun Wang, Wen Shi, Dynamics of Intraguild Predation Systems with Intraspecific Competition, 2018, 80, 0092-8240, 2408, 10.1007/s11538-018-0467-6
    4. Richard C. Bruce, Intraguild Interactions and Population Regulation in Plethodontid Salamanders, 2008, 22, 0733-1347, 31, 10.1655/07-015.1
    5. K. Blue Pahl, David J. Yurkowski, Kirsty J. Lees, Nigel E. Hussey, Measuring the occurrence and strength of intraguild predation in modern food webs, 2020, 25, 23522496, e00165, 10.1016/j.fooweb.2020.e00165
    6. Melanie J. Hatcher, Jaimie T. A. Dick, Alison M. Dunn, How parasites affect interactions between competitors and predators, 2006, 9, 1461-023X, 1253, 10.1111/j.1461-0248.2006.00964.x
    7. Yuanshi Wang, Hong Wu, Population dynamics of intraguild predation in a lattice gas system, 2015, 259, 00255564, 1, 10.1016/j.mbs.2014.11.001
    8. Zhiguang Liu, Fengpan Zhang, Species coexistence of communities with intraguild predation: The role of refuges used by the resource and the intraguild prey, 2013, 114, 03032647, 25, 10.1016/j.biosystems.2013.07.010
    9. Yun Kang, Lauren Wedekin, Dynamics of a intraguild predation model with generalist or specialist predator, 2013, 67, 0303-6812, 1227, 10.1007/s00285-012-0584-z
    10. Yuanshi Wang, Donald L. DeAngelis, Stability of an intraguild predation system with mutual predation, 2016, 33, 10075704, 141, 10.1016/j.cnsns.2015.09.004
    11. Gaku Takimoto, Takeshi Miki, Maiko Kagami, Intraguild predation promotes complex alternative states along a productivity gradient, 2007, 72, 00405809, 264, 10.1016/j.tpb.2007.04.005
    12. Richard J. Hall, Intraguild predation in the presence of a shared natural enemy, 2011, 92, 0012-9658, 352, 10.1890/09-2314.1
    13. Kejun Zhuang, Hongjun Yuan, Spatiotemporal dynamics of a predator–prey system with prey-taxis and intraguild predation, 2019, 2019, 1687-1847, 10.1186/s13662-019-1945-3
    14. Manuel Falconi, Yrina Vera-Damián, Claudio Vidal, Predator interference in a Leslie–Gower intraguild predation model, 2020, 51, 14681218, 102974, 10.1016/j.nonrwa.2019.102974
    15. Yiding Yang, Zhilan Feng, Dashun Xu, Gregory J. Sandland, Dennis J. Minchella, Evolution of host resistance to parasite infection in the snail–schistosome–human system, 2012, 65, 0303-6812, 201, 10.1007/s00285-011-0457-x
    16. Suparna Dash, Subhas Khajanchi, Dynamics of intraguild predation with intraspecies competition, 2023, 1598-5865, 10.1007/s12190-023-01956-7
    17. Emanuel A. Fronhofer, Lynn Govaert, Mary I. O'Connor, Sebastian J. Schreiber, Florian Altermatt, The shape of density dependence and the relationship between population growth, intraspecific competition and equilibrium population density, 2023, 0030-1299, 10.1111/oik.09824
    18. Purnedu Mishra, Dariusz Wrzosek, Schoener-Polis-Holt's model of the intraguild predation with predator taxis and repulsive chemotaxis, 2024, 0, 1531-3492, 0, 10.3934/dcdsb.2024062
    19. Debjit Pal, Dipak Kesh, Debasis Mukherjee, Study of a diffusive intraguild predation model, 2025, 2, 2997-6006, 10.20935/AcadEnvSci7508
    20. Jiang Li, Xianning Liu, Yangjiang Wei, Multistable switches induced by prudent predation in three-species food web models with omnivory, 2025, 198, 09600779, 116577, 10.1016/j.chaos.2025.116577
  • Reader Comments
  • © 2020 the Author(s), licensee AIMS Press. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0)
通讯作者: 陈斌, bchen63@163.com
  • 1. 

    沈阳化工大学材料科学与工程学院 沈阳 110142

  1. 本站搜索
  2. 百度学术搜索
  3. 万方数据库搜索
  4. CNKI搜索

Metrics

Article views(7212) PDF downloads(216) Cited by(2)

Figures and Tables

Figures(1)  /  Tables(3)

Other Articles By Authors

/

DownLoad:  Full-Size Img  PowerPoint
Return
Return

Catalog