Loading [MathJax]/jax/element/mml/optable/SuppMathOperators.js
Mini review

Interleukin-6 targeting antibodies for the treatment of Myelin Oligodendrocyte Glycoprotein Antibody-associated Disease (MOGAD): A review of current literature

  • These two authors contributed equally.
  • Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is an autoimmune inflammatory demyelinating disorder that can manifest as optic neuritis, transverse myelitis, and acute disseminated encephalomyelitis. Although typically monophasic, relapsing cases are more common in adults. Current treatments include corticosteroids, intravenous immunoglobulin, immune-suppressive drugs, and plasma exchange, but there is emerging interest in the use of interleukin-6 (IL-6) inhibitors to prevent relapses such as tocilizumab and satralizumab. This review analyzed 24 studies on IL-6 inhibitors for MOGAD, including case reports, case series, and retrospective studies with at least one MOGAD patient. Tocilizumab demonstrated significant efficacy, with most studies reporting reduced annualized relapse rates (ARR), prolonged relapse-free periods, and improved neurological outcomes, including stabilization or recovery of vision, motor function, and magnetic resonance imaging (MRI) lesion resolution. Satralizumab also showed potential, though data were more limited. While IL-6 inhibitors appear beneficial for steroid-dependent or treatment-resistant MOGAD, the existing data are limited to small, observational studies. Larger controlled trials are needed to establish their long-term efficacy and safety.

    Citation: Siddarth R. Ganesh, Orion Yedidia, Krupa Pandey, Carmenrita Infortuna, Charitha Madiraju, Florian P. Thomas, Fortunato Battaglia. Interleukin-6 targeting antibodies for the treatment of Myelin Oligodendrocyte Glycoprotein Antibody-associated Disease (MOGAD): A review of current literature[J]. AIMS Neuroscience, 2025, 12(2): 113-139. doi: 10.3934/Neuroscience.2025008

    Related Papers:

    [1] Wei Shi, Xinguang Yang, Xingjie Yan . Determination of the 3D Navier-Stokes equations with damping. Electronic Research Archive, 2022, 30(10): 3872-3886. doi: 10.3934/era.2022197
    [2] Jie Qi, Weike Wang . Global solutions to the Cauchy problem of BNSP equations in some classes of large data. Electronic Research Archive, 2024, 32(9): 5496-5541. doi: 10.3934/era.2024255
    [3] Guoliang Ju, Can Chen, Rongliang Chen, Jingzhi Li, Kaitai Li, Shaohui Zhang . Numerical simulation for 3D flow in flow channel of aeroengine turbine fan based on dimension splitting method. Electronic Research Archive, 2020, 28(2): 837-851. doi: 10.3934/era.2020043
    [4] Jie Zhang, Gaoli Huang, Fan Wu . Energy equality in the isentropic compressible Navier-Stokes-Maxwell equations. Electronic Research Archive, 2023, 31(10): 6412-6424. doi: 10.3934/era.2023324
    [5] Keqin Su, Rong Yang . Pullback dynamics and robustness for the 3D Navier-Stokes-Voigt equations with memory. Electronic Research Archive, 2023, 31(2): 928-946. doi: 10.3934/era.2023046
    [6] Linlin Tan, Bianru Cheng . Global well-posedness of 2D incompressible Navier–Stokes–Darcy flow in a type of generalized time-dependent porosity media. Electronic Research Archive, 2024, 32(10): 5649-5681. doi: 10.3934/era.2024262
    [7] Xiao Su, Hongwei Zhang . On the global existence and blow-up for the double dispersion equation with exponential term. Electronic Research Archive, 2023, 31(1): 467-491. doi: 10.3934/era.2023023
    [8] Wanxun Jia, Ling Li, Haoyan Zhang, Gengxiang Wang, Yang Liu . A novel nonlinear viscous contact model with a Newtonian fluid-filled dashpot applied for impact behavior in particle systems. Electronic Research Archive, 2025, 33(5): 3135-3157. doi: 10.3934/era.2025137
    [9] Guochun Wu, Han Wang, Yinghui Zhang . Optimal time-decay rates of the compressible Navier–Stokes–Poisson system in R3. Electronic Research Archive, 2021, 29(6): 3889-3908. doi: 10.3934/era.2021067
    [10] Xu Zhao, Wenshu Zhou . Vanishing diffusion limit and boundary layers for a nonlinear hyperbolic system with damping and diffusion. Electronic Research Archive, 2023, 31(10): 6505-6524. doi: 10.3934/era.2023329
  • Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is an autoimmune inflammatory demyelinating disorder that can manifest as optic neuritis, transverse myelitis, and acute disseminated encephalomyelitis. Although typically monophasic, relapsing cases are more common in adults. Current treatments include corticosteroids, intravenous immunoglobulin, immune-suppressive drugs, and plasma exchange, but there is emerging interest in the use of interleukin-6 (IL-6) inhibitors to prevent relapses such as tocilizumab and satralizumab. This review analyzed 24 studies on IL-6 inhibitors for MOGAD, including case reports, case series, and retrospective studies with at least one MOGAD patient. Tocilizumab demonstrated significant efficacy, with most studies reporting reduced annualized relapse rates (ARR), prolonged relapse-free periods, and improved neurological outcomes, including stabilization or recovery of vision, motor function, and magnetic resonance imaging (MRI) lesion resolution. Satralizumab also showed potential, though data were more limited. While IL-6 inhibitors appear beneficial for steroid-dependent or treatment-resistant MOGAD, the existing data are limited to small, observational studies. Larger controlled trials are needed to establish their long-term efficacy and safety.



    The insurance company is a common financial institution in our real life. Its profit mainly comes from two aspects: premium income and investment income, and the risks it needs to face mainly include: compensation risk and investment risk. In the past decade, more and more scholars have focused on building appropriate risk models (r.m.) to describe the various situations that insurance companies may face[1,2,3]. At first, the r.m. studied by the researchers was a classical risk model that only considered a company's claims as a negative jump. For example, Zhang et al.[4] studied a new method to estimate the Gerber-Shiu discount penalty function (p.f.) under the classical r.m., and Peng et al.[5] studied a r.m. of dividend payment with perturbations. But in reality, an insurance company's random returns should also be taken into account. To better fit the actual situation, Boucheire et al.[6] first proposed the two-sided jumps r.m., which is used to extend the r.m. of a single jump. Here, it is considered that the company's revenue is random, which is also a random variable, then the random revenue is a non-negative jump, and a negative jump is a claim. Since then, this model has been paid much attention by many researchers. For example, E.C.K. Cheung[7] studied a renewal model with continuous expenses and bidirectional jumps, where the amplitude of the jumps and the time intervals of arrival time are random. From this, E.C.K. Cheung obtained the updated equation of the discounted penalty funtion (e.d.p.f.) with defects. Zhang[8] considered the problem of e.d.p.f. for a two-sided jumps r.m. with dividend payout and obtained some explicit expressions. Wang et al. [9] considered the investment r.m. under the bilateral jump and tried to obtain the maximum surplus through the appropriate investment proportion. Xu et al.[10] studied the problem of ruin probability under bilateral jumps with random observations. For more research on two-side jump r.m., we can refer to references [11,12,13,14,15].

    Subsequently, some scholars put forward the dividend barrier strategy, that is, they set a threshold value b>0, and pay dividends to shareholders when the company's earnings are greater than b. The strategy was first proposed by De Finetti. Then, Gerber et al.[16] studied the threshold dividend strategy, and Yin et al.[17] and Cossette et al.[18] put forward the horizontal barrier strategy. The multi-tier dividend strategy can be learned from Xie and Zou[19]. To make the r.m. more realistic, some scholars have added dividend barriers to the study of bilateral jump risk models. For example, Bo et al. [20] studied the Lévy model with bilateral jumps under the dividend barrier strategy and Chen et al.[21] studied the dividend payment and the reward and e.d.p.f. of the dividend strategy with a threshold under the compound Poisson (c.p.) model. The integral differential equation (IDE) is derived under the boundary conditions and the approximate solution (a.s.) is approximated by the sinc numerical method. When studying the c.p. model with proportional investment, Chen and Ou[21] added the dividend with threshold value. Inspired by the above research, we propose a bilateral jumps model with a threshold strategy under random observation.

    We introduce our work in the following parts. In the second section, we construct the two-sided jumps risk model with investment interest under random observation, and the observational intervals obey a same exponential distribution. In the third section, we obtain the IDE of the expected discounted dividend payment (e.d.d.p.) function. To solve this equation, in the fourth section, we introduce an excellent numerical method to the solution of the IDEs and get the upper boundary of the error between the a.s. and the real solution. This numerical method is called the sinc numerical method. In the last section, we give some numerical examples to explore the effects of the included parameters on the e.d.d.p..

    According to the previous research on the bilateral jump r.m., we define

    U(t)=u0+ctS1t+S2t=u0+ctM1(t)i=1Yi+M2(t)i=1Zi,   t0, (2.1)

    where u0 represents the company's initial surplus on the account and u0 is greater than zero. In addition, {U(t)}t0 stands for the surplus process, while c represents the premium rate paid by the insured, so obviously c>0. Here the two stochastic processes S1t=M1(t)i=1Yi and S2t=M2(t)i=1Zi, are both c.p. processes, representing the total claims and returns until time t, respectively, and M1(t) and M2(t) are homogeneous Poisson processes with parameters λ1>0 and λ2>0. The claim size is determined by the cumulative distribution function (c.d.f.) FY() and the probability density function (p.d.f.) fY() of independent and identically distributed (i.i.d.) positive random variables (r.v.s) {Yi}i=1. The random return is given by the c.d.f. FZ() and the p.d.f. fZ() of the positive r.v.s {Zi}i=1. Define M1(t)=sup{j:S11+S12++S1jt} and M2(t)=sup{j:S21+S22++S2jt}, where inter-claim times {S1j}j=1 and inter-return times {S2j}j=1 follow the exponential distribution of intensity λ1 and λ2, respectively.

    In reality, to protect the interests of the manager and the insured, the manager needs to have a reasonable plan for the surplus funds. Under normal circumstances, insurance companies generally take a portfolio of risk and risk-free investments for surplus funds[22]. As investment income becomes a larger share of insurance company's total revenue, we need to take into account investment ratio factors. Therefore, suppose that the manager uses part of the surplus funds for risk-free investment and the other part for risk investment. In that way, risk-free investment {Rt}t0 satisfies

    dRtRt=rdt, (2.2)

    where r is the interest rate on a risk-free asset, so obviously r should be greater than zero. Risk asset {Qt}t0 is defined as

    Qt=eσWt+at, (2.3)

    where {Wt,t0} is a standard Brownian motion, and σ and a represent the volatility and expected rate of return of risk assets, respectively, both of which are greater than zero. So the risk asset process {Qt}t0 satisfies

    dQtQt=(a+12σ2)dt+σdWt. (2.4)

    Let q(0,1) represent the proportion of the insurance company's surplus invested in risky assets, and then 1q represents the proportion invested in risk-free assets. So U(t) satisfies

    dU(t)=qU(t)dQtQt+(1q)U(t)dRtRt+cdtdS1t+dS2t=qσU(t)dWt+(c+ξU(t))dtdM1(t)i=1Yi+dM2(t)i=1Zi, (2.5)

    where ξ=(a+12σ2)q+(1q)r, U(t) is the left limit of U(t) at t, and the loading condition to ensure that the formula holds is c+λ2E[Z1]>λ1E[Y1].

    We consider the dividend problems of the above model under the dividend strategy: when U(t) is greater than threshold b, dividends are paid consecutively in α, where α is constant and greater than zero; when U(t) is greater than zero and less than b>0, no dividends are paid; and when U(t) is less than zero, bankruptcy occurs at this time (but, in practice, the state of this moment may not be observed and therefore is still meaningful in the short term). Combined with Eq (2.5), the surplus process with threshold b is represented by {Ub(t),t0}, and {Ub(t),t0} satisfies

    dUb(t)={Ub(t)V(Q,R,q,t)+cdtdS1t+dS2t,           <Ub(t)0,Ub(t)V(Q,R,q,t)+cdtdS1t+dS2t,            0<Ub(t)b,Ub(t)V(Q,R,q,t)+(cα)dtdS1t+dS2t,  b<Ub(t)<, (2.6)

    where V(Q,R,q,t)=(1q)dRtRt+qdQtQt.

    Let the cumulative dividend paid until the ruin time t be D(t), and Tb=inf{t:Ub(t)0} is the ruin time. The present value of accumulated dividends before the ruin time Tb is Du,b, so

    Du,b=Tb0eδtdD(t)=αTb0I(Ub(t)>b)eδtdt, (2.7)

    where δ is the interest force and is greater than zero, and I() stands for the indicator function. According to the above definition, it is not difficult to derive 0<Du,b<αδ, which provides convenience for the subsequent derivation of the boundary of the IDEs. For uR, the expectation of Du,b is represented by

    V(u;b)=E[Du,b|Ub(0)=u]. (2.8)

    It should be emphasized that the surplus can be observed randomly in this paper. In practice, however, the executive director of an insurance company randomly reviews the balance of the company's books to determine whether dividends are being paid or whether it is ruined (e.g., [23,24,25]). Suppose {Tj}j=0 is a series of discrete time points of the moments of observing surplus, where Tj is the jth observation time. In addition, we stipulate that T0=0 and Tj is the time when the company goes to ruin, where j=inf{j1:M(j)0}. Suppose {Sj}j=0 is an i.i.d sequence, where Sj=TjTj1 is the jth observation interval and Sj are positive r.v.s, which are subject to an exponential distribution of intensity γ>0. Suppose {Yi}i=1, {Zi}i=1, {M1(t)}t0, {M2(t)}t0, {Wt,t0}, and {Sj}j=0 are independent of each other. Let the surplus level of the jth observation be M(j)=U(Tj), and combine (2.5) to obtain

    M(j)=M(j1)+TjTj1qσM(t)dWt+TkTk1(ξM(t)+c)dtTjTj1dM1(t)i=1Yi+TjTj1dM2(t)i=1Zi. (2.9)

    In this section, our work is to give the IDEs of e.d.d.p. V(u;b). Before we begin, we need to discuss the range of values of u, considering a time interval (0,dt]. If a claim occurred before observation, it is possible that Ub(t)<0 was not observed. Therefore, the range of values of u extends to the entire field of real numbers. In addition, it is not difficult to find that for different initial surplus u, V(u;b) behaves differently. For convenience, let us set

    V(u;b)={V1(u;b),  u(,0],V2(u;b),  u(0,b],V3(u;b),  u(b,).

    Here are the following conclusions.

    Theorem 3.1. For u(,0], V1(u;b) satisfies

    12q2u2σ2V1(u;b)+(ξu+c)V1(u;b)(λ1+λ2+δ)V1(u;b)+λ10V1(uy;b)dFY(y)+λ2[u0V1(u+z;b)dFZ(z)+u+buV2(u+z;b)dFZ(z)+u+bV3(u+z;b)dFZ(z)]=0. (3.1)

    For u(0,b], V2(u;b) satisfies

    12q2u2σ2V2(u;b)+(ξu+c)V2(u;b)(δ+λ1+λ2)V2(u;b)+λ1[u0V2(uy;b)dFY(y)+uV1(uy;b)dFY(y)]+λ2[bu0V2(u+z;b)dFZ(z)+buV3(u+z;b)dFZ(z)]=0, (3.2)

    and for u(b,), V3(u;b) satisfies

    12q2u2σ2V3(u;b)+(ξu+cα)V3(u;b)(δ+λ1+λ2)V3(u;b)+λ1[ub0V3(uy;b)dFY(y)+uubV2(uy;b)dFY(y)+uV1(uy;b)dFY(y)]+λ20V3(u+z;b)dFZ(z)+α=0. (3.3)

    The following boundary conditions are satisfied

    limuV1(u;b)=0; (3.4)
    limu+V3(u;b)=αδ; (3.5)
    V2(b;b)=V3(b+;b); (3.6)
    V2(b;b)=V3(b+;b). (3.7)

    Proof. Consider an infinitesimal interval (0, dt], and discuss whether claims and benefits occur or not. The cumulative distribution function of Yi and Zi is continuous. For u(,0],

    V1(u,b)=eδdt{γdtP0E[V1(h1t;b)]+(1γdt)P0E[V1(h1t;b)]+(1γdt)P1E[E[V1(h1t+Z1;b)|0<Z1<u]+E[V2(h1t+Z1;b)|u<Z1<bh1t]+E[V3(h1t+Z1;b)|bh1t<Z1]]+γdtP1E[V1(h1t+Z1;b)]+(1γdt)P2E[V1(h1tY1;b)]+γdtP2E[V1(h1tY1;b)]}, (3.8)

    and for u(0,b],

      V2(u,b)=eδdt{γdtP0E[V2(h1t;b)]+(1γdt)P0E[V2(h1t;b)]+(1γdt)P1E[E[V2(h1t+Z1;b)|u<Z1<bh1t]+E[V3(h1t+Z1;b)|bh1t<Z1]]+γdtP1E[V2(h1t+Z1;b)]+(1γdt)P2E[E[V2(h1tY1;b)|h1tb<Y1<u]+E[V1(h1tY1;b)|u<Y1]]+γdtP2E[V2(h1tY1;b)]}, (3.9)

    amd for u(b,),

    V3(u,b)=eδdt{αdt+γdtP0E[V3(h2t;b)]+(1γdt)P0E[V3(h2t;b)]+(1γdt)P2E[E[V1(h1tY1;b)|u<Y1]+E[V2(h1tY1;b)|h1tb<Y1<u]+E[V3(h2tY1;b)|0<Y1<h1tb]]+γdtE[V3(h2tY1;b)]+(1γdt)P1E[V3(h2t+Z1;b)]+γdtP1E[V3(h2t+Z1;b)]}, (3.10)

    where

    P0=P(S11>dt,S21>dt)=1(λ1+λ2)dt+o(dt), (3.11)
    P1=P(S11>dt,S21dt)=λ2dt+o(dt), (3.12)
    P2=P(S11dt,S21>dt)=λ1dt+o(dt). (3.13)

    According to the Itô formula, we get

    E[V1(h1t;b)]=E[V1(u;b)+(ξu+c)V1(u;b)dt+12q2u2σ2V1(u;b)dt]+o(dt), (3.14)
    E[V2(h1t;b)]=E[V2(u;b)+(ξu+c)V2(u;b)dt+12q2u2σ2V2(u;b)dt]+o(dt), (3.15)
    E[V3(h2t;b)]=E[V3(u;b)+(ξu+cα)V3(u;b)dt+12q2u2σ2V3(u;b)dt]+o(dt), (3.16)

    where

    h1t=u+quσdWt+(ξu+k)dt, (3.17)
    h2t=u+quσdWt+(ξu+kα)dt, (3.18)

    and o(dt) stands for the infinitesimal of higher order dt.

    Substitute Eqs (3.11)–(3.14) into Eqs (3.8)–(3.10), respectively. Divide both sides of the equation by dt and let dt approach zero infinitely. According to the properties of higher order infinitesimals and some careful calculation, we can get the IDEs (3.1)–(3.3).

    With further analysis, if the initial surplus Ub<0, the ruin occurs immediately, at which time no dividend is paid; then Tb=0. If 0<Ub<b, then the ruin did not occur and the dividend is always paid at rate α. If Ub>b, then the shares are always paid at rates αc, so Tb=.

    Remark 3.1. Referring to the analysis of Albrecher [26], we can also find that V(u;b) is not differentiable when u=0 in general. Similarly, to fully describe the solution of Theorem 3.1, we also use V1(0;b)=V2(0+;b) and V1(b;b)=V2(b+;b), and the boundary conditions (3.4) and (3.5).

    The sinc numerical method was proposed by James H. Wilkinson in the 1950s and developed by Frank Stenger in the 1990s. Frank Stenger summarized his work results in [27], which caused a great response in various fields (e.g., [28,29]). The real solutions to Eqs (3.1)–(3.3) are theoretically difficult to obtain. Therefore, we changed the angle, tried to obtain the a.s. by a numerical method, and then carried out an error analysis. Nowadays, the commonly used numerical methods for solving integral differential equations include the RK-Fehlberg method, the sinc method, the Runge-Kutta method, the Adams method, and so on. The sinc numerical method has high accuracy and good convergence when the sampling interval is small enough, which makes it perform well in high-precision numerical results. At the same time, the sinc method has an adaptive sampling interval. When the sampling interval is small, the sinc method can accurately reflect the details of the original function, to achieve high-precision numerical calculation. When the sampling interval is large, the sinc method can effectively smooth the function and avoid the ringing effect [30] in the interpolation process. Therefore, we also use this numerical method here.

    Since the domain of u is the entire real axis, in order to construct approximations on R, we consider conformal mappings. According to Algorithm 1.5.18 of Stenger[27], we define an injective mapping from RR

    ϕ(z)=z, (4.1)

    where zR. Define the grid point zk of sinc as

    zk=ϕ1(kh)=kh, (k=0,±1,±2,),

    where kZ, h>0. Based on the sinc method, the basis function of zΓ on the interval (,) is given by the following composite function

    Cj(z)=C(j,h)ϕ(z)=sinc(ϕ(z)jhh).

    Following the steps of the sinc method, we arrange Eqs (3.1)–(3.3) into the following integral differential

    12q2u2σ2V(u;b)+(ξu+cαIu>b)V(u;b)(λ1+λ2+δ)V(u;b)+0λ1V(uy;b)dFY(y)+0λ2V(u+z;b)dFZ(z)+αI(u>b)=0. (4.2)

    By the nature of convolution, Eq (4.2) is rewritten as

    12q2u2σ2V(u;b)+(ξu+cαIu>b)V(u;b)(λ1+λ2+δ)V(u;b)+uλ1V(y;b)fY(uy)dy++uλ2V(z;b)fZ(zu)dz+αI(u>b)=0. (4.3)

    According to formulas (3.4) and (3.5), and Definition 1.5.2 in reference[27], we have

    h(u;b)=v(t1;b)+ζ(u)v(t2;b)1+ζ(u),

    where ζ(u)=eϕ(u)=eu, when t1, t2. Set

    W(u)=V(u;b)h(u;b)=V(u;b)eu1+euαδ, (4.4)

    and then W(u)L˜α,˜β(δ), where L˜α,˜β(δ) is the function space for the sinc approximation over the finite interval (˜α,˜β) (p. 72 in [27]).

    V(u;b)=h(u;b)+W(u)=W(u)+eu1+euαδ, (4.5)
    V(u;b)=h(u;b)+W(u)=W(u)+eu(1+eu)2αδ, (4.6)
    V(u;b)=h(u;b)+W(u)=W(u)+eu(1eu)(1+eu)3αδ. (4.7)

    When u, u

    limuW(u)=0;limu+W(u)=0.

    Substituting (4.5)–(4.7) into (4.3), by simple calculation, we have

    μ0(u)W(u)+μ1(u)W(u)+μ2(u)W(u)+λ1uW(y)K1(uy)dy+λ2uW(z)K2(zu)dz+f(u)=0, (4.8)

    where μ0(u)=(quδ)22, μ1(u)=ξu+cαI(u>b), μ2(u)=(δ+λ1+λ2),

    K1(uy)=fY(uy), (4.9)
    K2(zu)=fZ(zu), (4.10)
    f(u)=αIu>b+μ0(u)eu(1eu)(1+eu)3αδ+μ1(u)eu(1+eu)2αδ+μ2(u)eu1+euαδ           +λ1uey1+eyαδK1(uy)dy+λ2uez1+ezαδK2(zu)dz. (4.11)

    When h>0, define the sinc grid point as

    uk=kh, k=±1,±2,. (4.12)

    Then consulting reference [27], according to Theorem 1.5.13, Theorem 1.5.14, and Theorem 1.5.20, we can get

    uK1(uy)W(y)dyn1j=n2n1i=n2ωiAijUj, (4.13)
    uK2(zu)W(z)dzn1j=n2n1i=n2ωiBijUj, (4.14)
    W(u)˜W(u)=n1j=n2UjC(j,h)ϕ(x), (4.15)

    where A and B are resemble diagonal matrices Λ, with Aij and Bij denoting the elements at (i,j) in A and B, respectively. The approximate value of W(uj) is expressed by Uj.

    Substituting (4.13)–(4.15) into Eq (4.8), replacing the integral term on the right side of Eq (4.8) with Eqs (4.13)–(4.15), and replacing u with uk for k=n2,,n1, where uk is the sinc grid point, we have

    μ0(uk)˜W(uk)+μ1(uk)˜W(uk)+μ2(uk)˜W(uk)+λ1n1j=n2n1i=n2ωi(uk)AijUj+λ2n1j=n2n1i=n2ωi(uk)BijUj=f(uk), (4.16)

    where

    ˜W(uk)=n1j=n2Uj[C(j,h)ϕ(uk)]=n1j=n2Ujδ(0)jk, (4.17)
    ˜W(uk)=n1j=n2Uj[C(j,h)ϕ(uk)]=n1j=n2Ujϕ(uk)δ(1)jk, (4.18)
    ˜W(uk)=n1j=n2Uj[C(j,h)ϕ(uk)]=n1j=n2Uj[ϕ(uk)h1δ(1)jk+[ϕ(uk)]2h2δ(2)jk]. (4.19)

    Substituting (4.17)–(4.19) into Eq (4.16), we have

    n1j=n2Uj{μ0(uk)(ϕ(uk)δ(1)jkh+(ϕ(uk))2δ(2)jkh2)+μ1(uk)ϕ(uk)δ(1)jkh+μ2(uk)δ(0)jk+λ1n1i=n2ωi(uk)Aij+λ2n1i=n2ωi(uk)Bij}=f(uk). (4.20)

    Multiplying Eq (4.20) by h2[ϕ(uk)]2, we have

    n1j=n2Uj{μ0(uk)δ(2)jk+h[μ0(uk)ϕ(uk)[ϕ(uk)]2+μ1(uk)ϕ(uk)]δ(1)jk+h2μ2(uk)[ϕ(uk)]2δ(0)jk+λ1h2[ϕ(uk)]2n1i=n2ωi(uk)Aij+λ2h2[ϕ(uk)]2n1i=n2ωi(uk)Bij}=f(uk)h2[ϕ(uk)]2. (4.21)

    Since

    δ(0)jk=δ(0)kj,    δ(1)jk=δ(1)kj,    δ(2)jk=δ(2)kj, and  ϕ(xk)ϕ(uk)2=(1ϕ(uk)),

    formula (4.21) can be turned into

    n1j=n2Uj{μ0(uk)δ(2)kj+h[μ0(uk)ϕ(uk)[ϕ(uk)]2+μ1(uk)ϕ(uk)]δ(1)kj+h2μ2(uk)[ϕ(uk)]2δ(0)kj+λ1h2[ϕ(uk)]2n1i=n2ωi(uk)Aij+λ2h2[ϕ(uk)]2n1i=n2ωi(uk)Bij}=f(uk)h2[ϕ(uk)]2. (4.22)

    Set I(m)=[δ(m)kj](n2+n1+1)×(n2+n1+1), and m=1,0,1,2. We rewrite Eq (4.22) as

    GU=F, (4.23)

    where

    U=[Uj]T=[Un2,,Un1]T,F=[h2f(un2)ϕ(un2)2,,h2f(un1)(ϕ(un1))2],G=μ0I(2)+hDm(μ0(1ϕ)μ1ϕ)I(1)+h2Dm(μ2ϕ2)I(0)+λ1h2Dm(1(ϕ)2)ΩmA   +λ2h2Dm(1(ϕ)2)ΩmB.

    So solving Eq (4.23), we get the expression of the approximate solution (a.s) of (4.5):

    V(u;b)=W(u)+eu1+euαδ˜W(u)+eu1+euαδ=n1j=n2UjC(j,h)ϕ(u)+eu1+euαδ. (4.24)

    The meanings of the symbols mentioned in the above process are shown in Table 1.

    Table 1.  Symbol specification.
    n1 positive integer
    n2 [n1˜β˜α]
    Dm(f) diag[f(Zn2),,f(Zn1)]
    Ωm (ωn2,ωn2+1,,ωn11,ωn1)
    ωn2 (1+en2h)[11+ρn1j=(n21)γj1+ejh]
    ωn1 (1+en1h)[ρ1+ρn11j=n2eijγj1+ejh]
    ωn2 11+ρn1j=(n21)γj1+ejh
    ωn1 ρ1+ρn11j=n2eijγj1+ejh
    ωj C(j,h)ϕ, j=n1+1,,n21
    γj C(j,h)ϕ, j=n1,,n2

     | Show Table
    DownLoad: CSV

    In the previous subsection, we obtained an inexact solution (e.s.) of the IDEs by using the sinc method. Therefore, in this section, we need to analyze the discrepancy between the a.s.s and the actual solutions. According to references [27,31], we find an upper bound of the error. Moreover, in reality, u is non-negative. Therefore, in this subsection, our discussion takes place under the condition u>0. Multiply 1μ0(u) by both sides of Eq (4.8), and we set

    G(u)=λ1μ0(u)uW(y)K1(uy)dyλ2μ0(u)uW(z)K2(zu)dzf(u)μ0(u),

    so we have

    G(u)=~μ2(u)W(u)+~μ1(u)W(u)+W(u), (4.25)

    where ~μ1(u)=μ1(u)μ0(u), ~μ1(u)=μ2(u)μ0(u).

    Assumption 4.1. Let ~μ1(u)/ζ, 1/(ζ), and ~μ2(u)/(ζ)2 be elements of W(D), and we are given that G/(ζ)2Lˆα(D) and Eq (4.25) possess a single solution WLˆα(D).

    In the above assumption, W(D) represents the family of all functions of W(u) that are analytically and uniformly bounded by D, and Lˆα(D)=Lˆα,ˆα(D).

    Theorem 4.2. If the aforementioned assumption is true, W represents the e.s. of Eq (4.25), ˜W represents the a.s. of Eq (4.24), and U=(Un2, , Un1)T represents the e.s. of Eq (4.23). So there is a constant ˜c>0, and different from N, such that

    supuΓ|W(u)˜W(u)| (4.26)

    Proof. Let

    (4.27)

    By using the triangle inequality, it is easily obtained that

    (4.28)

    Based on Theorem 4.4 in [31], there is a constant , and different from , that according to Assumption 3.1, , and we have

    (4.29)

    For inequality (4.28), fulfills

    (4.30)

    Similar to Theorem 3.8 in [31], if , then , and we can obtain

    (4.31)

    where and that is not dependent on . Let us take , and therefore, inequality (4.25) is obtained by formulas (4.27) − (4.31).

    Through formulas (4.4), (4.24), and (4.25), we get

    (4.32)

    In this subsection, we provide specific numerical examples to demonstrate the effectiveness of the sinc method, and study the effects of investment ratio and fluctuation parameter on the expected discounted dividend payout under exponential and lognormal distributions, respectively.

    All numerical examples in this section are assumed to be obtained under

    and

    Then,

    (5.1)

    and

    (5.2)

    Formulas (4.8) and (4.11) are converted to

    (5.3)

    and

    (5.4)

    Next, we examine how parameters and affect . If not specified, the following example parameters are set as follows: , .

    Example 5.1. The effect of the investment ratio on the e.d.d.p. is considered in the case of the exponential distribution of claims and returns. Set parameter . As depicted in Figure 1, it becomes evident that as the proportion of surplus invested in risk assets increases, the corresponding fluctuation of also increases. The value of when changes is presented in Table 2 partially.

    Figure 1.  The change of with .
    Table 2.  The value of when changes.
    −0.5 0 0.5 1.0 1.5 2.0 2.5 3.0 3.5 4.0
    3.430 3.294 3.360 3.378 3.182 3.431 3.059 3.504 3.080 3.640 3.265
    3.575 3.242 3.442 3.537 3.080 3.733 2.810 3.931 2.830 4.205 3.184
    3.701 3.057 3.493 3.738 2.882 4.203 2.395 4.604 2.374 5.040 2.898
    3.806 2.707 3.494 3.982 2.559 4.869 1.773 5.565 1.656 66.198 2.325

     | Show Table
    DownLoad: CSV

    Example 5.2. The effect of volatility parameter on the e.d.d.p. is considered in the case of the exponential distribution of claims and returns. Set parameter . As depicted in Figure 2, the greater the change of parameter , the greater the fluctuation of the curve corresponding to . Partial data is presented in Table 3.

    Figure 2.  The change of with .
    Table 3.  The value of when changes.
    −0.5 0 0.5 1.0 1.5 2.0 2.5 3.0 3.5 4.0
    0.2 3.430 3.294 3.360 3.378 3.182 3.431 3.059 3.504 3.080 3.640 3.265
    0.3 3.575 3.118 3.936 2.999 3.883 2.879 3.712 3.001 3.484 3.484 3.605
    0.4 3.999 3.426 3.697 3.788 3.003 4.041 2.548 4.398 4.964 4.964 3.401
    0.5 4.385 3.476 3.921 4.086 2.852 4.517 2.147 5.091 5.962 5.962 3.444

     | Show Table
    DownLoad: CSV

    As can be seen from Examples 5.1 and 5.2, the impact of two factors on the e.d.d.p. is considered: the proportion of risk investment and the volatility of risk assets . First, when a company invests a higher proportion of its surplus in risky assets, the dividend payout is higher, but also more volatile, while the dividend payout is more stable when the investment ratio is lower. This means high risk, high reward, danger, and opportunity. In addition, if the proportion of risk investment is fixed, choosing investment products with more volatile risk assets will bring higher profits, but also bear higher risks. On the contrary, they will earn lower profits and take lower risks. This is in line with reality.

    In this section, it is assumed that and obey a lognormal distribution of parameter and , respectively, where and , and and represent the variance, so that and are defined as

    Then,

    (5.5)

    and

    (5.6)

    Therefore, the formulas (4.8) and (4.11) can be rewritten as:

    (5.7)

    and

    (5.8)

    The next example is given in real condition: , , , , , .

    Example 5.3. In the case of a lognormal distribution of claims and returns, let us discuss the effect of investment ratio on . Set parameter . It is not difficult to see from Figure 3 that when a company invests more surplus into risk assets, the growth of its expected discounted dividend curve experiences significant fluctuations. Partial data is presented in Table 4.

    Figure 3.  The change of with .
    Table 4.  The value of when changes.
    = 2.25 2.5 2.75 3.0 3.25 3.50 3.75 4.0 4.25 4.5
    0.2 1.697 1.873 2.064 2.190 2.273 2.394 2.533 2.565 2.437 2.241 2.052
    0.4 1.768 2.386 3.081 3.490 3.717 4.143 4.732 4.951 4.534 3.880 3.345
    0.6 1.846 3.086 4.541 5.285 5.552 6.349 7.686 8.293 7.466 6.161 5.335
    0.8 1.931 3.936 6.402 7.487 7.583 8.712 11.068 12.278 10.902 8.7263 7.734

     | Show Table
    DownLoad: CSV

    Example 5.4. In the case of a lognormal distribution of claims and returns, let us discuss the effect of investment ratio on . Set parameter . It is not difficult to see from Figure 4 that when the company chooses a product investment with greater risk fluctuation, the growth of its expected discounted dividend curve exhibits substantial variability. Partial data is presented in Table 5.

    Figure 4.  The change of with .
    Table 5.  The value of when changes.
    = 2.25 2.5 2.75 3.0 3.25 3.50 3.75 4.0 4.25 4.5
    0.2 1.697 1.873 2.064 2.190 2.273 2.394 2.533 2.565 2.437 2.241 2.052
    0.4 1.809 2.505 3.263 3.761 4.091 4.577 5.145 5.297 4.810 4.053 3.334
    0.6 1.968 3.487 5.156 6.226 6.915 7.981 9.280 9.671 8.626 6.996 5.493
    0.8 2.134 4.735 7.612 9.393 10.475 12.291 14.632 15.427 13.677 10.929 8.521

     | Show Table
    DownLoad: CSV

    From Examples 5.3 and 5.4, it can be seen that parameters and have different effects on the e.d.d.p. under a lognormal distribution of claims and returns. Other parameters being equal, the expected discounted dividend payout curve fluctuates more when a company invests a larger proportion of its earnings or invests in risky products with a higher freezing rate. It should be noted that when the claim amount and income follow the lognormal distribution, shows a higher sensitivity to the above parameter changes.

    We explore a model with two-sided jumps, incorporating random observations and a dividend barrier strategy. By referring to the existing relevant literature, we find that the existing research is the classic model with a dividend strategy or the two-sided jump risk model. We want to know the situation of the dividend barrier strategy under double risk. According to this idea, through the literature review, we find that the model has very important practical significance. At the same time, we find that no scholars have introduced random observation into this model, but this is exactly what is for random observation in real life. In the process of research, we also find that there is no closed solution to the integral differential equation of this model after introducing random observation. To solve this problem, we obtained an a.s. by the sinc numerical method and analyzed the upper limit of the error. Perhaps one day in the future, we will have a better way to find the e.s. to this model.

    Chunwei Wang: Methodology, supervision, resources, funding acquisition, writing-review & editing; Shaohua Li: Methodology, software, visualization, writing-original draft; Shujing Wang: Software, visualization; Jiaen Xu: Methodology, validation. All authors have read and agreed to the published version of the manuscript.

    The authors declare they have not used Artificial Intelligence (AI) tools in the creation of this article.

    The research was supported by the National Natural Science Foundation of China (No. 71801085). The authors would like to thank the referees for their valuable comments and suggestions.

    All authors declare no conflicts of interest in this paper.



    Conflict of interest



    The authors declare no conflicts of interest.

    Authors' contributions



    SRG, OY, KP, CM, and FB planned the literature search; SRG and OY performed the literature search and drafted the first version of the manuscript; KP, CM, and FB reviewed the methodology; SRG, OY, KP, CI, CM, FPT, and FB contributed to data interpretation; SRG, OY, KP, CI, CM, FPT, and FB revised the manuscript critically. All authors approved the final version of the manuscript.

    [1] Hor JY, Fujihara K (2023) Epidemiology of myelin oligodendrocyte glycoprotein antibody-associated disease: a review of prevalence and incidence worldwide. Front Neurol 14: 1260358. https://doi.org/10.3389/fneur.2023.1260358
    [2] Banwell B, Bennett JL, Marignier R, et al. (2023) Diagnosis of myelin oligodendrocyte glycoprotein antibody-associated disease: International MOGAD Panel proposed criteria. Lancet Neurol 22: 268-282. https://doi.org/10.1016/S1474-4422(22)00431-8
    [3] Fadda G, Flanagan EP, Cacciaguerra L, et al. (2022) Myelitis features and outcomes in CNS demyelinating disorders: comparison between multiple sclerosis, MOGAD, and AQP4-IgG-positive NMOSD. Front Neurol 13: 1011579. https://doi.org/10.3389/fneur.2022.1011579
    [4] Uzawa A, Oertel FC, Mori M, et al. (2024) NMOSD and MOGAD: an evolving disease spectrum. Nat Rev Neurol 20: 602-619. https://doi.org/10.1038/s41582-024-01014-1
    [5] Schoeps VA, Virupakshaiah A, Waubant E (2024) Unveiling the Performance of Proposed MOGAD Diagnostic Criteria. Neurology 103: e209551. https://doi.org/10.1212/WNL.0000000000209551
    [6] Bartels F, Lu A, Oertel FC, et al. (2021) Clinical and neuroimaging findings in MOGAD–MRI and OCT. Clin Exp Immunol 206: 266-281. https://doi.org/10.1111/cei.13641
    [7] Perez-Giraldo G, Caldito NG, Grebenciucova E (2023) Transverse myelitis in myelin oligodendrocyte glycoprotein antibody-associated disease. Front Neurol 14: 1210972. https://doi.org/10.3389/fneur.2023.1210972
    [8] Ciron J, Cobo-Calvo A, Audoin B, et al. (2020) Frequency and characteristics of short versus longitudinally extensive myelitis in adults with MOG antibodies: a retrospective multicentric study. Mult Scler 26: 936-944. https://doi.org/10.1177/1352458519849511
    [9] Sun X, Liu M, Luo X, et al. (2022) Clinical characteristics and prognosis of pediatric myelin oligodendrocyte glycoprotein antibody-associated diseases in China. BMC Pediatr 22: 666. https://doi.org/10.1186/s12887-022-03679-3
    [10] Armangue T, Olivé-Cirera G, Martínez-Hernandez E, et al. (2020) Associations of paediatric demyelinating and encephalitic syndromes with myelin oligodendrocyte glycoprotein antibodies: a multicentre observational study. Lancet Neurol 19: 234-246. https://doi.org/10.1016/S1474-4422(19)30488-0
    [11] Satukijchai C, Mariano R, Messina S, et al. (2022) Factors associated with relapse and treatment of myelin oligodendrocyte glycoprotein antibody–associated disease in the United Kingdom. JAMA Netw Open 5: e2142780. https://doi.org/10.1001/jamanetworkopen.2021.42780
    [12] Wolf AB, Palace J, Bennett JL (2023) Emerging principles for treating myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD). Curr Treat Option Ne 25: 437-453. https://doi.org/10.1007/s11940-023-00776-1
    [13] Lai QL, Zhang YX, Cai MT, et al. (2021) Efficacy and safety of immunosuppressive therapy in myelin oligodendrocyte glycoprotein antibody-associated disease: a systematic review and meta-analysis. Ther Adv Neurol Disord 14: 17562864211054157. https://doi.org/10.1177/17562864211054157
    [14] Lerch M, Bauer A, Reindl M (2023) The Potential Pathogenicity of Myelin Oligodendrocyte Glycoprotein Antibodies in the Optic Pathway. J Neuroophthalmol 43: 5-16. https://doi.org/10.1097/WNO.0000000000001772
    [15] Gontika MP, Anagnostouli MC (2018) Anti-Myelin Oligodendrocyte Glycoprotein and Human Leukocyte Antigens as Markers in Pediatric and Adolescent Multiple Sclerosis: on Diagnosis, Clinical Phenotypes, and Therapeutic Responses. Mult Scler Int 2018: 8487471. https://doi.org/10.1155/2018/8487471
    [16] Weber J, Bernsdorff N, Robinson T, et al. (2021) Diagnosis of multiple sclerosis in times of MOG and AQP4 autoantibody testing - A monocentric study. J Neurol Sci 421: 117289. https://doi.org/10.1016/j.jns.2020.117289
    [17] Sheppard M, Laskou F, Stapleton PP, et al. (2017) Tocilizumab (actemra). Hum Vaccin Immunother 13: 1972-1988. https://doi.org/10.1080/21645515.2017.1316909
    [18] Schirmer M, Muratore F, Salvarani C (2018) Tocilizumab for the treatment of giant cell arteritis. Expert Rev Clin Immunol 14: 339-349. https://doi.org/10.1080/1744666X.2018.1468251
    [19] Si S, Teachey DT (2020) Spotlight on tocilizumab in the treatment of CAR-T-cell-induced cytokine release syndrome: clinical evidence to date. Ther Clin Risk Manag 16: 705-714. https://doi.org/10.2147/TCRM.S223468
    [20] Heo YA (2020) Satralizumab: First Approval. Drugs 80: 1477-1482. https://doi.org/10.1007/s40265-020-01380-2
    [21] Zhang C, Zhang M, Qiu W, et al. (2020) Safety and efficacy of tocilizumab versus azathioprine in highly relapsing neuromyelitis optica spectrum disorder (TANGO): an open-label, multicentre, randomised, phase 2 trial. Lancet Neurol 19: 391-401. https://doi.org/10.1016/S1474-4422(20)30070-3
    [22] Sbragia E, Boffa G, Varaldo R, et al. (2024) An aggressive form of MOGAD treated with aHSCT: A case report. Mult Scler 30: 612-616. https://doi.org/10.1177/13524585231213792
    [23] Masuccio FG, Lo Re M, Bertolotto A, et al. (2020) Benign SARS-CoV-2 infection in MOG-antibodies associated disorder during tocilizumab treatment. Mult Scler Relat Disord 46: 102592. https://doi.org/10.1016/j.msard.2020.102592
    [24] McLendon LA, Gambrah-Lyles C, Viaene A, et al. (2023) Dramatic Response to Anti-IL-6 Receptor Therapy in Children With Life-Threatening Myelin Oligodendrocyte Glycoprotein-Associated Disease. Neurol Neuroimmunol Neuroinflamm 10: e200150. https://doi.org/10.1212/NXI.0000000000200150
    [25] Kwon O, Choi J (2024) Effective Prevention with Maintenance Treatment of Tocilizumab in Pediatric MOG-IgG Associated Disorder (MOGAD) Relapse. Ann Child Neurol 32: 197-200. https://doi.org/10.26815/acn.2024.00514
    [26] Kang YR, Kim KH, Hyun JW, et al. (2024) Efficacy of tocilizumab in highly relapsing MOGAD with an inadequate response to intravenous immunoglobulin therapy: A case series. Mult Scler Relat Disord 91: 105859. https://doi.org/10.1016/j.msard.2024.105859
    [27] Elsbernd PM, Hoffman WR, Carter JL, et al. (2021) Interleukin-6 inhibition with tocilizumab for relapsing MOG-IgG associated disorder (MOGAD): A case-series and review. Mult Scler Relat Disord 48: 102696. https://doi.org/10.1016/j.msard.2020.102696
    [28] Kim S, Kim S, Jang Y, et al. (2023) Leptomeningeal Enhancement, a Phenotype of Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease With Caudate Nucleus Involvement: A Case Report and Literature Review. J Clin Neurol 19: 210-213. https://doi.org/10.3988/jcn.2022.0307
    [29] Virupakshaiah A, Moseley CE, Elicegui S, et al. (2024) Life-Threatening MOG Antibody-Associated Hemorrhagic ADEM With Elevated CSF IL-6. Neurol Neuroimmunol Neuroinflamm 11: e200243. https://doi.org/10.1212/NXI.0000000000200243
    [30] Lee Y, Ahn SJ, Lee HS, et al. (2023) Myelin oligodendrocyte glycoprotein antibody-associated encephalitis after severe acute respiratory syndrome coronavirus 2 infection: a case report and retrospective case reviews. Encephalitis 3: 71-77. https://doi.org/10.47936/encephalitis.2022.00129
    [31] Nagahata K, Suzuki S, Yokochi R, et al. (2022) Recurrent Optic Perineuritis With Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease Complicated With Granulomatous Polyangiitis. Cureus 14: e25239. https://doi.org/10.7759/cureus.25239
    [32] Smoot K, Chen C, Cohan S (2021) Recurrent relapse after 20 years in a patient with MOG antibody disease: A case report. Neuroimmunol Rep 1: 100042. https://doi.org/10.1016/j.nerep.2021.100042
    [33] Kroenke E, Ankar A, Malani Shukla N (2022) Refractory MOG-Associated Demyelinating Disease in a Pediatric Patient. Child Neurol Open 9: 2329048X221079093. https://doi.org/10.1177/2329048X221079093
    [34] Novi G, Gastaldi M, Franciotta D, et al. (2019) Tocilizumab in MOG-antibody spectrum disorder: a case report. Mult Scler Relat Disord 27: 312-314. https://doi.org/10.1016/j.msard.2018.11.012
    [35] Schirò G, Iacono S, Salemi G, et al. (2024) The pharmacological management of myelin oligodendrocyte glycoprotein-immunoglobulin G associated disease (MOGAD): an update of the literature. Expert Rev Neurother 24: 985-996. https://doi.org/10.1080/14737175.2024.2385941
    [36] Hayward-Koennecke H, Reindl M, Martin R, et al. (2019) Tocilizumab treatment in severe recurrent anti-MOG-associated optic neuritis. Neurology 92: 765-767. https://doi.org/10.1212/WNL.0000000000007312
    [37] Dayrit KC, Chua-Ley EO (2024) Use of Tocilizumab Followed by Rituximab Desensitization on Relapsing Myelin Oligodendrocyte Antibody Disease: A Case Report. Cureus 16: e52374. https://doi.org/10.7759/cureus.52374
    [38] Bilodeau PA, Vishnevetsky A, Molazadeh N, et al. (2024) Effectiveness of immunotherapies in relapsing myelin oligodendrocyte glycoprotein antibody-associated disease. Mult Scler 30: 357-368. https://doi.org/10.1177/13524585241226830
    [39] Lotan I, Charlson RW, Ryerson LZ, et al. (2020) Effectiveness of subcutaneous tocilizumab in neuromyelitis optica spectrum disorders. Mult Scler Relat Disord 39: 101920. https://doi.org/10.1016/j.msard.2019.101920
    [40] Rempe T, Rodriguez E, Elfasi A, et al. (2024) Frequency, characteristics, predictors and treatment of relapsing myelin oligodendrocyte glycoprotein antibody–associated disease (MOGAD). Mult Scler Relat Disord 87: 105672. https://doi.org/10.1016/j.msard.2024.105672
    [41] Ringelstein M, Ayzenberg I, Lindenblatt G, et al. (2021) Interleukin-6 receptor blockade in treatment-refractory MOG-IgG–associated disease and neuromyelitis optica spectrum disorders. Neurol Neuroimmunol Neuroinflamm 9: e1100. https://doi.org/10.1212/NXI.0000000000001100
    [42] Guzmán J, Vera F, Soler B, et al. (2023) Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease (MOGAD) in Chile: lessons learned from challenging cases. Mult Scler Relat Disord 69: 104442. https://doi.org/10.1016/j.msard.2022.104442
    [43] Rigal J, Pugnet G, Ciron J, et al. (2020) Off-label use of tocilizumab in neuromyelitis optica spectrum disorders and MOG-antibody-associated diseases: A case-series. Mult Scler Relat Disord 46: 102483. https://doi.org/10.1016/j.msard.2020.102483
    [44] Powers JH, Mooneyham GC (2020) Psychiatric Symptoms in Pediatric Patients With Myelin-Oligodendrocyte-Glycoprotein-Immunoglobulin G-Antibody Positive Autoimmune Encephalitis: A Case Series. Psychosomatics 61: 846-850. https://doi.org/10.1016/j.psym.2019.12.002
    [45] Jelcic I, Hanson JV, Lukas S, et al. (2019) Unfavorable structural and functional outcomes in myelin oligodendrocyte glycoprotein antibody–associated optic neuritis. J Neuroophthalmol 39: 3-7. https://doi.org/10.1097/WNO.0000000000000669
    [46] Hutto SK, Cavanagh JJ (2025) Advances in Diagnosis and Management of Atypical Demyelinating Diseases. Med Clin North Am 109: 425-441. https://doi.org/10.1016/j.mcna.2024.09.011
    [47] Schirò G, Iacono S, Andolina M, et al. (2023) Tocilizumab treatment in MOGAD: a case report and literature review. Neurol Sci 45: 1429-1436. https://doi.org/10.1007/s10072-023-07189-7
    [48] Schett G (2018) Physiological effects of modulating the interleukin-6 axis. Rheumatology (Oxford) 57: ii43-ii50. https://doi.org/10.1093/rheumatology/kex513
    [49] Yoshida Y, Tanaka T (2014) Interleukin 6 and rheumatoid arthritis. Biomed Res Int 2014: 698313. https://doi.org/10.1155/2014/698313
    [50] Tackey E, Lipsky PE, Illei GG (2004) Rationale for interleukin-6 blockade in systemic lupus erythematosus. Lupus 13: 339-343. https://doi.org/10.1191/0961203304lu1023oa
    [51] Koutsouraki E, Hatzifilipou E, Michmizos D, et al. (2011) Increase in interleukin-6 levels is related to depressive phenomena in the acute (relapsing) phase of multiple sclerosis. J Neuropsychiatry Clin Neurosci 23: 442-448. https://doi.org/10.1176/jnp.23.4.jnp442
    [52] Schneider A, Long SA, Cerosaletti K, et al. (2013) In active relapsing-remitting multiple sclerosis, effector T cell resistance to adaptive T(regs) involves IL-6-mediated signaling. Sci Transl Med 5: 170ra15. https://doi.org/10.1126/scitranslmed.3004970
    [53] Fujihara K, Bennett JL, de Seze J, et al. (2020) Interleukin-6 in neuromyelitis optica spectrum disorder pathophysiology. Neurol Neuroimmunol Neuroinflamm 7: e841. https://doi.org/10.1212/NXI.0000000000000841
    [54] Takeshita Y, Fujikawa S, Serizawa K, et al. (2021) New BBB Model Reveals That IL-6 Blockade Suppressed the BBB Disorder, Preventing Onset of NMOSD. Neurol Neuroimmunol Neuroinflamm 8: e1076. https://doi.org/10.1212/NXI.0000000000001076
    [55] Haramati A, Rechtman A, Zveik O, et al. (2022) IL-6 as a marker for NMOSD disease activity. J Neuroimmunol 370: 577925. https://doi.org/10.1016/j.jneuroim.2022.577925
    [56] Corbali O, Chitnis T (2023) Pathophysiology of myelin oligodendrocyte glycoprotein antibody disease. Front Neurol 14: 1137998. https://doi.org/10.3389/fneur.2023.1137998
    [57] Yao M, Wang W, Sun J, et al. (2024) The landscape of PBMCs in AQP4-IgG seropositive NMOSD and MOGAD, assessed by high dimensional mass cytometry. CNS Neurosci Ther 30: e14608. https://doi.org/10.1111/cns.14608
    [58] Horellou P, de Chalus A, Giorgi L, et al. (2021) Regulatory T Cells Increase After rh-MOG Stimulation in Non-Relapsing but Decrease in Relapsing MOG Antibody-Associated Disease at Onset in Children. Front Immunol 12: 679770. https://doi.org/10.3389/fimmu.2021.679770
    [59] Moseley CE, Virupakshaiah A, Forsthuber TG, et al. (2024) MOG CNS Autoimmunity and MOGAD. Neurol Neuroimmunol Neuroinflamm 11: e200275. https://doi.org/10.1212/NXI.0000000000200275
    [60] Whittam DH, Karthikeayan V, Gibbons E, et al. (2020) Treatment of MOG antibody associated disorders: results of an international survey. J Neurol 267: 3565-3577. https://doi.org/10.1007/s00415-020-10026-y
    [61] Nepal G, Kharel S, Coghlan MA, et al. (2022) Safety and efficacy of rituximab for relapse prevention in myelin oligodendrocyte glycoprotein immunoglobulin G (MOG-IgG)-associated disorders (MOGAD): A systematic review and meta-analysis. J Neuroimmunol 364: 577812. https://doi.org/10.1016/j.jneuroim.2022.577812
    [62] Yong KP, Kim HJ (2021) Demystifying MOGAD and Double Seronegative NMOSD Further With IL-6 Blockade. Neurol Neuroimmunol Neuroinflamm 9: e1110. https://doi.org/10.1212/NXI.0000000000001110
    [63] Cochrane LibrarySafety and Efficacy of Tocilizumab in Patients With Myelin Oligodendrocyte Glycoprotein Antibody-associated Disease, NCT06452537 (2024). [cited 2025 May 08]. Available from: https://www.cochranelibrary.com/central/doi/10.1002/central/CN-02709117/full
    [64] Cochrane LibraryA Study to Evaluate the Efficacy, Safety, Pharmacokinetics, and Pharmacodynamics of Satralizumab in Patients With Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease, NCT05271409 (2022). [cited 2025 May 08]. Available from: https://www.cochranelibrary.com/central/doi/10.1002/central/CN-02374734/full
    [65] Kothur K, Wienholt L, Tantsis EM, et al. (2016) B Cell, Th17, and Neutrophil Related Cerebrospinal Fluid Cytokine/Chemokines Are Elevated in MOG Antibody Associated Demyelination. PLoS One 11: e0149411. https://doi.org/10.1371/journal.pone.0149411
  • Reader Comments
  • © 2025 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(215) PDF downloads(21) Cited by(0)

Figures and Tables

Figures(1)  /  Tables(2)

/

DownLoad:  Full-Size Img  PowerPoint
Return
Return

Catalog