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

Spleen in innate and adaptive immunity regulation

  • Received: 27 October 2020 Accepted: 08 December 2020 Published: 10 December 2020
  • The spleen is a large secondary lymphoid organ located in the blood-stream, primarily functioning as a massive blood filter. It filtered effete red blood cells, antigen-antibody complexes, apoptotic bodies, damaged cells, among others. Spleen's myriad microanatomy reflects the diversity and complexity of its functions. As a specialized immune organ, the spleen immune system plays a significant role in innate and adaptive immunity. Specialized innate immune cells like B cells, natural killer (NK) cells, and macrophages populate locations within the spleen. Specifically, the spleen is a crucial organ for peripheral immune tolerance, complementing central immune tolerance. Spleen remains the only organ in the body capable of mounting an appropriate immune response to encapsulated bacteria. Spleen houses tolerogenic immune cells like CD8+ Treg cells, F4/80+ macrophages, CD68+F4/80+ red pulp macrophages, CD169+ metallophillic macrophages, CD8+CD205+ splenic dendritic cells (DCs), splenic CD8α+CD103+CD207+ DCs, CD43+veCD19hiCD5+veIgMhiIgDlo B cells, and splenic NKT cells that express regulated on activation normal T cell expressed and secreted (RANTES/CCL5) chemokine. Splenocytes are extra-thymic autoimmune regulator gene (AIRE) expressing cells that regulate tissue-specific antigens' expression to confer peripheral immune tolerance. As such, the spleen provides the right site for counteracting autoimmunity. Splenectomy in both study animals and humans results in overwhelming infections with, especially encapsulated bacteria. The anterior chamber-associated immune deviation (ACAID) is closely related to the spleen that needs to be studied to improve transplant survival. The role of the spleen in anti-tumor immunity yields an inconclusive result. In-depth research is needed to find which cells or pathways are linked to favorable outcomes concerning cancer. Understanding the spleen's microanatomy and physiology will provide a framework for treating diseases, especially autoimmune diseases, cancer, infections, and transplantation.

    Citation: Mansur Aliyu, Fatema Zohora, Ali Akbar Saboor-Yaraghi. Spleen in innate and adaptive immunity regulation[J]. AIMS Allergy and Immunology, 2021, 5(1): 1-17. doi: 10.3934/Allergy.2021001

    Related Papers:

    [1] Hanpeng Gao, Yunlong Zhou, Yuanfeng Zhang . Sincere wide $ \tau $-tilting modules. Electronic Research Archive, 2025, 33(4): 2275-2284. doi: 10.3934/era.2025099
    [2] Rongmin Zhu, Tiwei Zhao . The construction of tilting cotorsion pairs for hereditary abelian categories. Electronic Research Archive, 2025, 33(5): 2719-2735. doi: 10.3934/era.2025120
    [3] Yajun Ma, Haiyu Liu, Yuxian Geng . A new method to construct model structures from left Frobenius pairs in extriangulated categories. Electronic Research Archive, 2022, 30(8): 2774-2787. doi: 10.3934/era.2022142
    [4] Haiyu Liu, Rongmin Zhu, Yuxian Geng . Gorenstein global dimensions relative to balanced pairs. Electronic Research Archive, 2020, 28(4): 1563-1571. doi: 10.3934/era.2020082
    [5] Dongxing Fu, Xiaowei Xu, Zhibing Zhao . Generalized tilting modules and Frobenius extensions. Electronic Research Archive, 2022, 30(9): 3337-3350. doi: 10.3934/era.2022169
    [6] Agustín Moreno Cañadas, Robinson-Julian Serna, Isaías David Marín Gaviria . Zavadskij modules over cluster-tilted algebras of type $ \mathbb{A} $. Electronic Research Archive, 2022, 30(9): 3435-3451. doi: 10.3934/era.2022175
    [7] Shengxiang Wang, Xiaohui Zhang, Shuangjian Guo . The Hom-Long dimodule category and nonlinear equations. Electronic Research Archive, 2022, 30(1): 362-381. doi: 10.3934/era.2022019
    [8] Jiangsheng Hu, Dongdong Zhang, Tiwei Zhao, Panyue Zhou . Balance of complete cohomology in extriangulated categories. Electronic Research Archive, 2021, 29(5): 3341-3359. doi: 10.3934/era.2021042
    [9] Xiu-Jian Wang, Jia-Bao Liu . Quasi-tilted property of generalized lower triangular matrix algebras. Electronic Research Archive, 2025, 33(5): 3065-3073. doi: 10.3934/era.2025134
    [10] János Kollár . Relative mmp without $ \mathbb{Q} $-factoriality. Electronic Research Archive, 2021, 29(5): 3193-3203. doi: 10.3934/era.2021033
  • The spleen is a large secondary lymphoid organ located in the blood-stream, primarily functioning as a massive blood filter. It filtered effete red blood cells, antigen-antibody complexes, apoptotic bodies, damaged cells, among others. Spleen's myriad microanatomy reflects the diversity and complexity of its functions. As a specialized immune organ, the spleen immune system plays a significant role in innate and adaptive immunity. Specialized innate immune cells like B cells, natural killer (NK) cells, and macrophages populate locations within the spleen. Specifically, the spleen is a crucial organ for peripheral immune tolerance, complementing central immune tolerance. Spleen remains the only organ in the body capable of mounting an appropriate immune response to encapsulated bacteria. Spleen houses tolerogenic immune cells like CD8+ Treg cells, F4/80+ macrophages, CD68+F4/80+ red pulp macrophages, CD169+ metallophillic macrophages, CD8+CD205+ splenic dendritic cells (DCs), splenic CD8α+CD103+CD207+ DCs, CD43+veCD19hiCD5+veIgMhiIgDlo B cells, and splenic NKT cells that express regulated on activation normal T cell expressed and secreted (RANTES/CCL5) chemokine. Splenocytes are extra-thymic autoimmune regulator gene (AIRE) expressing cells that regulate tissue-specific antigens' expression to confer peripheral immune tolerance. As such, the spleen provides the right site for counteracting autoimmunity. Splenectomy in both study animals and humans results in overwhelming infections with, especially encapsulated bacteria. The anterior chamber-associated immune deviation (ACAID) is closely related to the spleen that needs to be studied to improve transplant survival. The role of the spleen in anti-tumor immunity yields an inconclusive result. In-depth research is needed to find which cells or pathways are linked to favorable outcomes concerning cancer. Understanding the spleen's microanatomy and physiology will provide a framework for treating diseases, especially autoimmune diseases, cancer, infections, and transplantation.


    In [1] (see [2] for type A), the authors introduced cluster categories which were associated to finite dimensional hereditary algebras. It is well known that cluster-tilting theory gives a way to construct abelian categories from some triangulated and exact categories.

    Recently, Nakaoka and Palu introduced extriangulated categories in [3], which are a simultaneous generalization of exact categories and triangulated categories, see also [4,5,6]. Subcategories of an extriangulated category which are closed under extension are also extriangulated categories. However, there exist some other examples of extriangulated categories which are neither exact nor triangulated, see [6,7,8].

    When T is a cluster tilting subcategory, the authors Yang, Zhou and Zhu [9, Definition 3.1] introduced the notions of T[1]-cluster tilting subcategories (also called ghost cluster tilting subcategories) and weak T[1]-cluster tilting subcategories in a triangulated category C, which are generalizations of cluster tilting subcategories. In these works, the authors investigated the relationship between C and modT via the restricted Yoneda functor G more closely. More precisely, they gave a bijection between the class of T[1]-cluster tilting subcategories of C and the class of support τ-tilting pairs of modT, see [9, Theorems 4.3 and 4.4].

    Inspired by Yang, Zhou and Zhu [9] and Liu and Zhou [10], we introduce the notion of relative cluster tilting subcategories in an extriangulated category B. More importantly, we want to investigate the relationship between relative cluster tilting subcategories and some important subcategories of modΩ(T)_ (see Theorem 3.9 and Corollary 3.10), which generalizes and improves the work by Yang, Zhou and Zhu [9] and Liu and Zhou [10].

    It is worth noting that the proof idea of our main results in this manuscript is similar to that in [9, Theorems 4.3 and 4.4], however, the generalization is nontrivial and we give a new proof technique.

    Throughout the paper, let B denote an additive category. The subcategories considered are full additive subcategories which are closed under isomorphisms. Let [X](A,B) denote the subgroup of HomB(A,B) consisting of morphisms which factor through objects in a subcategory X. The quotient category B/[X] of B by a subcategory X is the category with the same objects as B and the space of morphisms from A to B is the quotient of group of morphisms from A to B in B by the subgroup consisting of morphisms factor through objects in X. We use Ab to denote the category of abelian groups.

    In the following, we recall the definition and some properties of extriangulated categories from [4], [11] and [3].

    Suppose there exists a biadditive functor E:Bop×BAb. Let A,CB be two objects, an element δE(C,A) is called an E-extension. Zero element in E(C,A) is called the split E-extension.

    Let s be a correspondence, which associates any E-extension δE(C,A) to an equivalence class s(δ)=[AxByC]. Moreover, if s satisfies the conditions in [3, Definition 2.9], we call it a realization of E.

    Definition 2.1. [3, Definition 2.12] A triplet (B,E,s) is called an externally triangulated category, or for short, extriangulated category if

    (ET1) E:Bop×BAb is a biadditive functor.

    (ET2) s is an additive realization of E.

    (ET3) For a pair of E-extensions δE(C,A) and δE(C,A), realized as s(δ)=[AxByC] and s(δ)=[AxByC]. If there exists a commutative square,

    then there exists a morphism c:CC which makes the above diagram commutative.

    (ET3)op Dual of (ET3).

    (ET4) Let δ and δ be two E-extensions realized by AfBfD and BgCgF, respectively. Then there exist an object EB, and a commutative diagram

    and an E-extension δ realized by AhChE, which satisfy the following compatibilities:

    (i). DdEeF realizes E(F,f)(δ),

    (ii). E(d,A)(δ)=δ,

    (iii). E(E,f)(δ)=E(e,B)(δ).

    (ET4op) Dual of (ET4).

    Let B be an extriangulated category, we recall some notations from [3,6].

    ● We call a sequence XxYyZ a conflation if it realizes some E-extension δE(Z,X), where the morphism x is called an inflation, the morphism y is called an deflation and XxYyZδ is called an E-triangle.

    ●When XxYyZδ is an E-triangle, X is called the CoCone of the deflation y, and denote it by CoCone(y); C is called the Cone of the inflation x, and denote it by Cone(x).

    Remark 2.2. 1) Both inflations and deflations are closed under composition.

    2) We call a subcategory T extension-closed if for any E-triangle XxYyZδ with X, ZT, then YT.

    Denote I by the subcategory of all injective objects of B and P by the subcategory of all projective objects.

    In an extriangulated category having enough projectives and injectives, Liu and Nakaoka [4] defined the higher extension groups as

    Ei+1(X,Y)=E(Ωi(X),Y)=E(X,Σi(Y)) for i0.

    By [3, Corollary 3.5], there exists a useful lemma.

    Lemma 2.3. For a pair of E-triangles LlMmN and DdEeF. If there is a commutative diagram

    f factors through l if and only if h factors through e.

    In this section, B is always an extriangulated category and T is always a cluster tilting subcategory [6, Definition 2.10].

    Let A, BB be two objects, denote by [¯T](A,ΣB) the subset of B(A,ΣB) such that f[¯T](A,ΣB) if we have f: ATΣB where TT and the following commutative diagram

    where I is an injective object of B [10, Definition 3.2].

    Let M and N be two subcategories of B. The notation [¯T](M,Σ(N))=[T](M,Σ(N)) will mean that [¯T](M,ΣN)=[T](M,ΣN) for every object MM and NN.

    Now, we give the definition of T-cluster tilting subcategories.

    Definition 3.1 Let X be a subcategory of B.

    1) [11, Definition 2.14] X is called T-rigid if [¯T](X,ΣX)=[T](X,ΣX);

    2) X is called T-cluster tilting if X is strongly functorially finite in B and X={MC[¯T](X,ΣM)=[T](X,ΣM) and [¯T](M,ΣX)=[T](M,ΣX)}.

    Remark 3.2. 1) Rigid subcategories are always T-rigid by [6, Definition 2.10];

    2) T-cluster tilting subcategories are always T-rigid;

    3) T-cluster tilting subcategories always contain the class of projective objects P and injective objects I.

    Remark 3.3. Since T is a cluster tilting subcategory, XB, there exists a commutative diagram by [6, Remark 2.11] and Definition 2.1((ET4)op), where T1, T2T and h is a left T-approximation of X:

    Hence XB, there always exists an E-triangle

    Ω(T1)fXΩ(T2)X with TiT.

    By Remark 3.2(3), PT and B=CoCone(T,T) by [6, Remark 2.11(1),(2)]. Following from [4, Theorem 3.2], B_=B/T is an abelian category. fB(A,C), denote by f_ the image of f under the natural quotient functor BB_.

    Let Ω(T)=CoCone(P,T), then Ω(T)_ is the subcategory consisting of projective objects of B_ by [4, Theorem 4.10]. Moreover, modΩ(T)_ denotes the category of coherent functors over the category of Ω(T)_ by [4, Fact 4.13].

    Let G: BmodΩ(T)_, MHomB_(,M)Ω(T)_ be the restricted Yoneda functor. Then G is homological, i.e., any E-triangle XYZ in B yields an exact sequence G(X)G(Y)G(Z) in modΩ(T)_. Similar to [9, Theorem 2.8], we obtain a lemma:

    Lemma 3.4. Denote proj(modΩ(T)_) the subcategory of projective objects in modΩ(T)_. Then

    1) G induces an equivalence Ω(T)proj(modΩ(T)_).

    2) For NmodΩ(T)_, there exists a natural isomorphism

    HommodΩ(T)_(G(Ω(T)),N)N(Ω(T)).

    In the following, we investigate the relationship between B and modΩ(T)_ via G more closely.

    Lemma 3.5. Let X be any subcategory of B. Then

    1) any object XX, there is a projective presentation in mod Ω(T)_

    PG(X)1πG(X)PG(X)0G(X)0.

    2) X is a T-rigid subcategory if and only if the class {πG(X)XX} has property ((S) [9, Definition 2.7(1)]).

    Proof. 1). By Remark 3.3, there exists an E-triangle:

    Ω(T1)fXΩ(T0)X

    When we apply the functor G to it, there exists an exact sequence G(Ω(T1))G(Ω(T0))G(X)0. By Lemma 3.4(1), G(Ω(Ti)) is projective in mod Ω(T)_. So the above exact sequence is the desired projective presentation.

    2). For any X0X, using the similar proof to [9, Lemma 4.1], we get the following commutative diagram

    where α=HommodΩT_(πG(X),G(X0)). By Lemma 3.4(2), both the left and right vertical maps are isomorphisms. Hence the set {πG(X)XX} has property ((S) iff α is epic iff HomB_(fX,X0) is epic iff X is a T-rigid subcategory by [10, Lemma 3.6].

    Lemma 3.6. Let X be a T-rigid subcategory and T1 a subcategory of T. Then XT1 is a T-rigid subcategory iff E(T1,X)=0.

    Proof. For any MXT1, then M=XT1 for XX and T1T1. Let h: XT be a left T-approximation of X and y: T1Σ(X) for XX any morphism. Then there exists the following commutative diagram

    with P1P, f=(h001) and β=(i000i1).

    When XT1 is a T-rigid subcategory, we can get a morphism g: XT1Σ(X)Σ(T1) such that βg=(10)y(0 1)f. i.e., b: T1I such that y=i0b. So E(T1,X)=0 and then E(T1,X)=0.

    Let γ=(r11r12r21r22): TT1Σ(X)Σ(T1) be a morphism. As X is T-rigid, r11h: XΣ(X) factors through i0. Since E(T,X)=0, r12: T1Σ(X) factors through i0. As T is rigid, the morphism r21h: XTΣ(T1) factors through i1, and the morphism r22: T1Σ(T1) factors through i1. So the morphism γf can factor through β=(i000i1). Therefore XT1 is an T-rigid subcategory.

    For the definition of τ-rigid pair in an additive category, we refer the readers to see [9, Definition 2.7].

    Lemma 3.7. Let U be a class of T-rigid subcategories and V a class of τ-rigid pairs of modΩ(T)_. Then there exists a bijection φ: UV, given by : X(G(X),Ω(T)Ω(X)).

    Proof. Let X be T-rigid. By Lemma 3.5, G(X) is a τ-rigid subcategory of mod Ω(T)_.

    Let YΩ(T)Ω(X), then there exists X0X such that Y=Ω(X0). Consider the E-triangle Ω(X0)PX0 with PP. XX, applying HomB(,X) yields an exact sequence HomB(P,X)HomB(Ω(X0),X)E(X0,X)0. Hence in B_=B/T, HomB_(Ω(X0),X)E(X0,X).

    By Remark 3.3, for X0, there is an E-triangle Ω(T1)Ω(T2)X0 with T1, T2T. Applying HomB_(,X), we obtain an exact sequence HomB_(Ω(T2),X)HomB_(Ω(T1),X)E(X0,X)E(Ω(T2),X). By [10, Lemma 3.6], HomB_(Ω(T2),X)HomB_(Ω(T1),X) is epic. Moreover, Ω(T2)_ is projective in B_ by [4, Proposition 4.8]. So E(Ω(T2),X)=0. Thus E(X0,X)=0. Hence XX,

    G(X)(Y)=HomB_(Ω(X0),X)=0.

    So (G(X),Ω(T)Ω(X)) is a τ-rigid pairs of modΩ(T)_.

    We will show φ is a surjective map.

    Let (N,σ) be a τ-rigid pair of modΩ(T)_. NN, consider the projective presentation

    P1πNP0N0

    such that the class {πN|NN} has Property (S). By Lemma 3.4, there exists a unique morphism fN: Ω(T1)Ω(T0) in Ω(T)_ satisfying G(fN)=πN and G(Cone(fN))N. Following from Lemma 3.5, X1:= {cone(fN)NN} is a T-rigid subcategory.

    Let X=X1Y, where Y={TTΩ(T)σ}. For any T0Y, there is an E-triangle Ω(T0)PT0 with PP. For any Cone(fN)X1, applying HomB_(,Cone(fN)), yields an exact sequence HomB_(Ω(T0),Cone(fN))E(T0,Cone(fN))E(P,Cone(fN))=0. Since (N,σ) is a τ-rigid pair, HomB_(Ω(T0),Cone(fN))=G(Cone(fM))(Ω(T0))=0. So E(T0,Cone(fN))=0. Due to Lemma 3.6, X=X1Y is T-rigid. Since YT, we get G(Y)=HomB_(,T)Ω(T)=0 by [4, Lemma 4.7]. So G(X)=G(X1)=N.

    It is straightforward to check that Ω(T)Ω(X1)=0. Let XΩ(T)Ω(X), then XΩ(T) and XΩ(X)=Ω(X1)σ. So we can assume that X=Ω(X1)E, where Eσ. Then Ω(X1)EΩ(T). Since EΩ(T), we get Ω(X1)Ω(T)Ω(X1)=0. So Ω(T)Ω(X)σ. Clearly, σΩ(T). Moreover, σΩ(X). So σΩ(T)Ω(X). Hence Ω(T)Ω(X)=σ. Therefore φ is surjective.

    Lastly, φ is injective by the similar proof method to [9, Proposition 4.2].

    Therefore φ is bijective.

    Lemma 3.8. Let T be a rigid subcategory and AaBCδ an E-triangle satisfying [¯T](C,Σ(A))=[T](C,Σ(A)). If there exist an E-extension γE(T,A) and a morphism t: CT with TT such that tγ=δ, then the E-triangle AaBCδ splits.

    Proof. Applying HomB(T,) to the E-triangle AIiΣ(A)α with II, yields an exact sequence HomB(T,A)E(T,X)E(T,I)=0. So there is a morphism dHomB(T,Σ(A)) such that γ=dα. So δ=tγ=tdα=(dt)α. So we have a diagram which is commutative:

    Since [¯T](C,Σ(A))=[T](C,Σ(A)) and dt[T](C,Σ(A)), dt can factor through i. So 1A can factor through a and the result follows.

    Now, we will show our main theorem, which explains the relation between T-cluster tilting subcategories and support τ-tilting pairs of modΩ(T)_.

    The subcategory X is called a preimage of Y by G if G(X)=Y.

    Theorem 3.9. There is a correspondence between the class of T-cluster tilting subcategories of B and the class of support τ-tilting pairs of modΩ(T)_ such that the class of preimages of support τ-tilting subcategories is contravariantly finite in B.

    Proof. Let φ be the bijective map, such that X(G(X),Ω(TΩ(X))), where G is the restricted Yoneda functor defined in the argument above Lemma 3.4.

    1). The map φ is well-defined.

    If Xis T-cluster tilting, then X is T-rigid. So φ(X) is a τ-rigid pair of modΩ(T)_ by Lemma 3.7. Therefore Ω(T)Ω(X)KerG(X). Assume Ω(T0)Ω(T) is an object of KerG(X). Then HomB_(Ω(T0),X)=0. Applying HomB_(,X) with XX to Ω(T0)PT0 with PP, yields an exact sequence

    HomB_(P,X)HomB_(Ω(T),X)E(T0,X)0.

    Hence we get E(T0,X)HomB_(Ω(T0),X)=0.

    Applying HomB(T0,) to XIΣ(X), we obtain

    (3.1)      [¯T](T0,Σ(X))=[T](T0,Σ(X)).

    For any ba: XaRbΣ(T0) with RT, as T is rigid, we get a commutative diagram:

    Hence we get (3.2)[¯T](X,Σ(T0))=[T](X,Σ(T0)).

    By the equalities (3.1) and (3.2) and X being a T-rigid subcategory, we obtain

    [¯T](X,Σ(XT0))=[T](X,Σ(XT0)) and [¯T](XT0,Σ(X))=[T](XT0,Σ(X)).

    As X is T-cluster tilting, we get XT0X. So T0X. And thus Ω(T0)Ω(T)Ω(X). Hence KerG(X)=Ω(T)Ω(X).

    Since X is functorially finte, similar to [6, Lemma 4.1(2)], Ω(T)Ω(T), we can find an E-triangle Ω(T)fX1X2, where X1, X2X and f is a left X-approximation. Applying G, yields an exact sequence

    G(Ω(R))G(f)G(X1)G(X2)0.

    Thus we get a diagram which is commutative, where HomB_(f,X) is surjective.

    By Lemma 3.4, the morphism G(f) is surjective. So G(f) is a left G(X)-approximation and (G(X),Ω(T)Ω(X)) is a support τ-tilting pair of modΩ(T)_ by [3, Definition 2.12].

    2). φ is epic.

    Assume (N,σ) is a support τ-tilting pair of modΩ(T)_. By Lemma 3.7, there is a T-rigid subcategory X satisfies G(X)=N. So Ω(T)Ω((T)), there is an exact sequence G(Ω(T))αG(X3)G(X4)0, such that X3, X4X and α is a left G(X)-approximation. By Yoneda's lemma, we have a unique morphism in modΩ((T))_:

    β: Ω(T)X3 such that α=G(β) and G(cone(β))G(X4).

    Moreover, XX, consider the following commutative diagram

    By Lemma 3.4, G() is surjective. So the map HomB_(β,X) is surjective.

    Denote Cone(β) by YR and Xadd{YRΩ(T)Ω(T)} by ˜X.

    We claim ˜X is T-rigid.

    (I). Assume a: YRa1T0a2Σ(X) with T0T and XX. Consider the following diagram:

    Since X is T-rigid, f: X3I such that aγ=if. So there is a morphism g:Ω(T)X making the upper diagram commutative. Since HomB_(β,X) is surjective, g factors through β. Hence a factors through i, i.e., [¯T](YR,Σ(X))=[T](YR,Σ(X)).

    (II). For any morphism b: Xb1T0b2Σ(YR) with T0T and XX. Consider the following diagram:

    By [3, Lemma 5.9], RΣ(X3)Σ(YT) is an E-triangle. Because T is rigid, b2 factors through γ1. By the fact that X is T-rigid, b=b2b1 can factor through iX. Since γ1iX=iY, we get that b factors through iY. So [¯T](X,Σ(YT))=[T](X,Σ(YT)).

    By (I) and (II), we also obtain [¯T](YT,Σ(YT))=[T](YT,Σ(YT)).

    Therefore ˜X=Xadd{YTΩ(T)Ω(T)} is T-rigid.

    Let MB satisfying [¯T](M,Σ(˜X))=[T](M,Σ(˜X)) and [¯T](˜X,ΣM)=[T](˜X,ΣM). Consider the E-triangle:

    Ω(T5)fΩ(T6)gM

    where T5, T6T. By the above discussion, there exist two E-triangles:

    Ω(T6)uX6vY6 and Ω(T5)uX5vY5.

    where X5, X6X, u and u are left X-approximations of Ω(T6), Ω(T5), respectively. So there exists a diagram of E-triangles which is commutative:

    We claim that the morphism x=uf is a left X-approximation of Ω(T5). In fact, let XX and d: Ω(T5)X, we can get a commutative diagram of E-triangles:

    where PP. By the assumption, [¯T](M,Σ(X))=[T](M,Σ(X)). So d2h factors through iX. By Lemma 2.3, d factors through f. Thus f1: Ω(T6)X such that d=f1f. Moreover, u is a left X-approximation of Ω(T6). So u1: X6X such that f1=u1u. Thus d=f1f=u1uf=u1x. So x=uf is a left X-approximation of Ω(T5).

    Hence there is a commutative diagram:

    By [3, Corollary 3.16], we get an E-triangle X6(yλ)NX5Y5xδ5

    Since u is a left X-approximation of Ω(T5), there is also a commutative diagram with PP:

    such that δ5=tμ. So xδ5=xtμ=txμ. By Lemma 3.8, the E-triangle xδ5 splits. So NX5X6Y5˜X. hence N˜X.

    Similarly, consider the following commutative diagram with PP:

    and the E-triangle MNYgδ6. Then t: YT6 such that δ6=tδ. Then gδ6=gtδ=t(gδ). Since [¯T](˜X,ΣM)=[T](˜X,ΣM), the E-triangle gδ6 splits by Lemma 3.5 and M is a direct summands of N. Hence M˜X.

    By the above, we get ˜X is a T-cluster tilting subcategory.

    By the definition of YR, G(YR)G(X). So G(˜X)G(X)N. Moreover, σ=Ω(T)Ω(X)Ω(T)Ω(˜X) and Ω(T)Ω(˜X)kerG(X)=σ. So Ω(T)Ω(˜X)=σ. Hence φ is surjective.

    3). φ is injective following from the proof of Lemma 3.7.

    By [4, Proposition 4.8 and Fact 4.13], B_modΩ(T)_. So it is easy to get the following corollary by Theorem 3.9:

    Corollary 3.10. Let X be a subcategory of B.

    1) X is T-rigid iff X_ is τ-rigid subcategory of B_.

    2) X is T-cluster tilting iff X_ is support τ-tilting subcategory of B_.

    If let H=CoCone(T,T), then H can completely replace B and draw the corresponding conclusion by the proof Lemma 3.7 and Theorem 3.9, which is exactly [12, Theorem 3.8]. If let B is a triangulated category, then Theorem 3.9 is exactly [9, Theorem 4.3].

    This research was supported by the National Natural Science Foundation of China (No. 12101344) and Shan Dong Provincial Natural Science Foundation of China (No.ZR2015PA001).

    The authors declare they have no conflict of interest.



    Conflict of interests



    All authors declare no conflicts of interest in this paper.

    [1] Greer JP, Arber DA, Glader B, et al. (2013)  Wintrobes Clinical Hematology: Lymphocytes and Lymphatic Organs Philadelphia: Lippincott Williams & Wilkins, 227-410.
    [2] Haley PJ (2017) The lymphoid system: a review of species differences. Toxicol Pathol 30: 111-123. doi: 10.1293/tox.2016-0075
    [3] Dale DC (2016) The mysteries of the spleen. J Leukoc Biol 100: 249-251. doi: 10.1189/jlb.4CE0216-088R
    [4] Varga I, Babala J, Kachlik DJS, et al. (2018) Anatomic variations of the spleen: current state of terminology, classification, and embryological background. Surg Radiol Anat 40: 21-29. doi: 10.1007/s00276-017-1893-0
    [5] Endo A, Ueno S, Yamada S, et al. (2015) Morphogenesis of the spleen during the human embryonic period. Anat Rec 298: 820-826. doi: 10.1002/ar.23099
    [6] Ganusov VV, Tomura M (2018) Experimental and mathematical approaches to quantify recirculation kinetics of lymphocytes. BioRxiv .
    [7] Mebius RE, Kraal G (2005) Structure and function of the spleen. Nat Rev Immunol 5: 606-616. doi: 10.1038/nri1669
    [8] da Silva HB, Fonseca R, Pereira RM, et al. (2015) Splenic macrophage subsets and their function during blood-borne infections. Front Immunol 6: 480.
    [9] Premawardena C, Bowden D, Kaplan Z, et al. (2018) Understanding of the significance and health implications of asplenia in a cohort of patients with haemaglobinopathy: possible benefits of a spleen registry. Hematology 23: 526-530. doi: 10.1080/10245332.2017.1414910
    [10] Davidson R, Wall R (2001) Prevention and management of infections in patients without a spleen. Clin Microbiol Infect 7: 657-660. doi: 10.1046/j.1198-743x.2001.00355.x
    [11] Taniguchi LU, Correia MD, Zampieri FG (2014) Overwhelming post-splenectomy infection: narrative review of the literature. Surg Infect 15: 686-693. doi: 10.1089/sur.2013.051
    [12] Robier C, Schoberl M, Reiher H, et al. (2015) Bacteria on a peripheral blood smear as presenting sign of overwhelming post-splenectomy infection in a patient with secondary acute myeloid leukemia. Clin Chem Lab Med 53: e203-e205.
    [13] Leone G, Pizzigallo E (2015) Bacterial infections following splenectomy for malignant and nonmalignant hematologic diseases. Mediterr J Hematol Infect Dis 7: e2015057. doi: 10.4084/mjhid.2015.057
    [14] Ugel S, Peranzoni E, Desantis G, et al. (2012) Immune tolerance to tumor antigens occurs in a specialized environment of the spleen. Cell Rep 2: 628-639. doi: 10.1016/j.celrep.2012.08.006
    [15] Salminen A, Kauppinen A, Kaarniranta K (2018) Myeloid-derived suppressor cells (MDSC): an important partner in cellular/tissue senescence. Biogerontology 19: 325-339. doi: 10.1007/s10522-018-9762-8
    [16] Hwang HK, Murakami T, Kiyuna T, et al. (2017) Splenectomy is associated with an aggressive tumor growth pattern and altered host immunity in an orthotopic syngeneic murine pancreatic cancer model. Oncotarget 8: 88827-88834. doi: 10.18632/oncotarget.21331
    [17] Hwang HK, Kang CM, Lee SH, et al. (2018) Fluorescence-guided surgery with splenic preservation prevents tumor recurrence in an orthotopic nude-mouse model of human pancreatic cancer. Anticancer Res 38: 665-670.
    [18] Bronte V, Pittet MJ (2013) The spleen in local and systemic regulation of immunity. Immunity 39: 806-818. doi: 10.1016/j.immuni.2013.10.010
    [19] Sty JR, Conway JJ (1985) The spleen: development and functional evaluation. Semin Nucl Med 15: 276-298. doi: 10.1016/S0001-2998(85)80005-2
    [20] Chadburn A (2000) The spleen: anatomy and anatomical function. Semin Hematol 37: 13-21. doi: 10.1016/S0037-1963(00)90113-6
    [21] Papenfuss TL, Cesta MF (2017) Spleen. Immunopathology in Toxicology and Drug Development Cham: Humana Press, 37-57. doi: 10.1007/978-3-319-47385-7_2
    [22] Kage M, Kondou R, Ogata T (2019) Anatomy of the spleen and pathology of hypersplenism. Clinical Investigation of Portal Hypertension Singapore: Springer, 25-34. doi: 10.1007/978-981-10-7425-7_3
    [23] Steiniger BS (2015) Human spleen microanatomy: why mice do not suffice. Immunology 145: 334-346. doi: 10.1111/imm.12469
    [24] den Haan JM, Kraal G (2012) Innate immune functions of macrophage subpopulations in the spleen. J Innate Immun 4: 437-445. doi: 10.1159/000335216
    [25] Murphy K, Weaver C (2017) Basic concepts in immunology. Janeway's Immunobiology New York: Garland Science, 18-36.
    [26] Garraud O, Borhis G, Badr G, et al. (2012) Revisiting the B-cell compartment in mouse and humans: more than one B-cell subset exists in the marginal zone and beyond. BMC Immunol 13: 63. doi: 10.1186/1471-2172-13-63
    [27] Cesta MF (2006) Normal structure, function, and histology of the spleen. Toxicol Pathol 34: 455-465. doi: 10.1080/01926230600867743
    [28] Nus M, Sage AP, Lu Y, et al. (2017) Marginal zone B cells control the response of follicular helper T cells to a high-cholesterol diet. Nat Med 23: 601-610. doi: 10.1038/nm.4315
    [29] Turner VM, Mabbott NA (2017) Ageing adversely affects the migration and function of marginal zone B cells. Immunology 151: 349-362. doi: 10.1111/imm.12737
    [30] Shlomchik MJ, Weisel F (2012) Germinal center selection and the development of memory B and plasma cells. Immunol Rev 247: 52-63. doi: 10.1111/j.1600-065X.2012.01124.x
    [31] Steiniger B, Barth P (2000)  Microanatomy and Function of the Spleen Heidelberg: Springer. doi: 10.1007/978-3-642-57088-9
    [32] Kumar N, Patil J, Swamy RS, et al. (2014) Atypical arterial supply to the spleen by polar branches of splenic artery and accessory splenic artery—a case report. J Clin Diagnostic Res 8: AD03-AD04.
    [33] Groom AC, Schmidt EE, MacDonald IC (1991) Microcirculatory pathways and blood flow in spleen: new insights from washout kinetics, corrosion casts, and quantitative intravital videomicroscopy. Scanning Microsc 5: 159-174.
    [34] Steiniger BS, Ulrich C, Berthold M, et al. (2018) Capillary networks and follicular marginal zones in human spleens. Three-dimensional models based on immunostained serial sections. PLoS One 13: e0191019. doi: 10.1371/journal.pone.0191019
    [35] Pabst R (1988) The spleen in lymphocyte migration. Immunol Today 9: 43-45. doi: 10.1016/0167-5699(88)91258-3
    [36] Steiniger B, Timphus EM, Jacob R, et al. (2005) CD27+ B cells in human lymphatic organs: re-evaluating the splenic marginal zone. Immunology 116: 429-442.
    [37] Bickenbach KA, Gonen M, Labow DM, et al. (2013) Indications for and efficacy of splenectomy for haematological disorders. Br J Surg 100: 794-800. doi: 10.1002/bjs.9067
    [38] Coco D, Leanza S (2019) Indications for surgery in non-traumatic spleen disease. Open Access Maced J Med Sci 7: 2958-2960. doi: 10.3889/oamjms.2019.568
    [39] Fallah J, Olszewski AJ (2019) Diagnostic and therapeutic splenectomy for splenic lymphomas: analysis of the National Cancer Data Base. Hematology 24: 378-386. doi: 10.1080/16078454.2019.1591570
    [40] Huang L, Li W, Yang T, et al. (2020) Association between splenectomy and portal hypertension in the development of pulmonary hypertension. Pulm Circ 10: 1-9. doi: 10.1177/2045894019895426
    [41] Nagem RG, Petroianu A (2009) Subtotal splenectomy for splenic abscess. Can J Surg 52: E91-E92.
    [42] Luu S, Spelman D, Woolley IJ (2019) Post-splenectomy sepsis: preventative strategies, challenges, and solutions. Infect Drug Resist 12: 2839-2851. doi: 10.2147/IDR.S179902
    [43] Manciu S, Tudor S, Vasilescu C (2018) Splenic cysts: a strong indication for a minimally invasive partial splenectomy. Could the splenic hilar vasculature type hold a defining role? World J Surg 42: 3543-3550. doi: 10.1007/s00268-018-4650-6
    [44] Kraal G (1992) Cells in the marginal zone of the spleen. Int Rev Cytol 132: 31-74. doi: 10.1016/S0074-7696(08)62453-5
    [45] Kashimura M, Shibata A (1989) Structure and functions of the human spleen: relationship between microcirculation and splenic functions. Rinsho Ketsueki 30: 1234-1238.
    [46] Ram S, Lewis LA, Rice PA (2010) Infections of people with complement deficiencies and patients who have undergone splenectomy. Clin Microbiol Rev 23: 740-780. doi: 10.1128/CMR.00048-09
    [47] Sojka DK, Tian Z, Yokoyama WM (2014) Tissue-resident natural killer cells and their potential diversity. Semin Immunol 26: 127-131. doi: 10.1016/j.smim.2014.01.010
    [48] Peng H, Tian Z (2017) Diversity of tissue-resident NK cells. Semin Immunol 31: 3-10. doi: 10.1016/j.smim.2017.07.006
    [49] Spits H, Bernink JH, Lanier L (2016) NK cells and type 1 innate lymphoid cells: partners in host defense. Nat Immunol 17: 758-764. doi: 10.1038/ni.3482
    [50] Hadad U, Thauland TJ, Martinez OM, et al. (2015) NKp46 clusters at the immune synapse and regulates NK cell polarization. Front Immunol 6: 495-495. doi: 10.3389/fimmu.2015.00495
    [51] Robinette ML, Colonna M (2016) Innate lymphoid cells and the MHC. HLA 87: 5-11. doi: 10.1111/tan.12723
    [52] Tomaz D, Pereira PM, Guerra N, et al. (2018) Nanoscale colocalization of NK cell activating and inhibitory receptors controls signal integration. BioRxiv .
    [53] Ashouri E, Farjadian S, Reed EF, et al. (2009) KIR gene content diversity in four Iranian populations. Immunogenetics 61: 483-492. doi: 10.1007/s00251-009-0378-7
    [54] Wang HD, Jin XY, Guo YX, et al. (2019) KIR gene presence/absence polymorphisms and global diversity in the Kirgiz ethnic minority and populations distributed worldwide. Mol Biol Rep 46: 1043-1055. doi: 10.1007/s11033-018-4563-3
    [55] Osman AE, Mubasher M, ElSheikh NE, et al. (2014) Characterization of human killer immunoglobulin-like receptors (KIRs) among healthy Saudis. Hum Immunol 75: 536-540. doi: 10.1016/j.humimm.2014.02.023
    [56] Ricklin D, Reis ES, Mastellos DC, et al. (2016) Complement component C3—The “Swiss Army Knife” of innate immunity and host defense. Immunol Rev 274: 33-58. doi: 10.1111/imr.12500
    [57] Schechter MC, Satola SW, Stephens DS (2019) Host defenses to extracellular bacteria. Clin Immunol London: Elsevier, 391-402. doi: 10.1016/B978-0-7020-6896-6.00027-2
    [58] Ram S, Lewis LA, Rice PA (2010) Infections of people with complement deficiencies and patients who have undergone splenectomy. Clin Microbiol Rev 23: 740-780. doi: 10.1128/CMR.00048-09
    [59] Koppel EA, Saeland E, de Cooker DJ, et al. (2005) DC-SIGN specifically recognizes Streptococcus pneumoniae serotypes 3 and 14. Immunobiology 210: 203-210. doi: 10.1016/j.imbio.2005.05.014
    [60] Aichele P, Zinke J, Grode L, et al. (2003) Macrophages of the splenic marginal zone are essential for trapping of blood-borne particulate antigen but dispensable for induction of specific T cell responses. J Immunol 171: 1148-1155. doi: 10.4049/jimmunol.171.3.1148
    [61] Pluddemann A, Mukhopadhyay S, Sankala M, et al. (2009) SR-A, MARCO and TLRs differentially recognise selected surface proteins from Neisseria meningitidis: an example of fine specificity in microbial ligand recognition by innate immune receptors. J Innate Immun 1: 153-163. doi: 10.1159/000155227
    [62] Uy PPD, Francisco DM, Trivedi A, et al. (2017) Vascular diseases of the spleen: A review. J Clin Transl Hepatol 5: 152-164.
    [63] Pivkin IV, Peng Z, Karniadakis GE, et al. (2016) Biomechanics of red blood cells in human spleen and consequences for physiology and disease. Proc Natl Acad Sci USA 113: 7804-7809. doi: 10.1073/pnas.1606751113
    [64] Li H, Lu L, Li X, et al. (2018) Mechanics of diseased red blood cells in human spleen and consequences for hereditary blood disorders. Proc Natl Acad Sci USA 115: 9574-9579. doi: 10.1073/pnas.1806501115
    [65] Prasad A, Kumar SS, Dessimoz C, et al. (2013) Global regulatory architecture of human, mouse and rat tissue transcriptomes. BMC Genomics 14: 716. doi: 10.1186/1471-2164-14-716
    [66] Cook MC, Basten A, Groth BFDS (1997) Outer periarteriolar lymphoid sheath arrest and subsequent differentiation of both naive and tolerant immunoglobulin transgenic B cells is determined by B cell receptor occupancy. J Exp Med 186: 631-643. doi: 10.1084/jem.186.5.631
    [67] Wluka A, Olszewski WL (2006) Innate and adaptive processes in the spleen. Ann Transplant 11: 22-29.
    [68] Steinman RM, Pack M, Inaba K (1997) Dendritic cells in the T-cell areas of lymphoid organs. Immunol Rev 156: 25-37. doi: 10.1111/j.1600-065X.1997.tb00956.x
    [69] Chung JB, Silverman M, Monroe JG (2003) Transitional B cells: step by step towards immune competence. Trends Immunol 24: 343-349. doi: 10.1016/S1471-4906(03)00119-4
    [70] Chung JB, Sater RA, Fields ML, et al. (2002) CD23 defines two distinct subsets of immature B cells which differ in their responses to T cell help signals. Int Immunol 14: 157-166. doi: 10.1093/intimm/14.2.157
    [71] Yilma M (2018) Review on immune tolerance mechanism and physiology. Glob J Med Res 18: 12-17.
    [72] Buettner M, Bornemann M, Bode U (2013) Skin tolerance is supported by the spleen. Scand J Immunol 77: 238-245. doi: 10.1111/sji.12034
    [73] Ding J, Liu S, Zhang D, et al. (2018) Transfusion of ethylene carbodiimide-fixed donor splenocytes prolongs survival of vascularized skin allografts. J Surg Res 221: 343-352. doi: 10.1016/j.jss.2017.06.005
    [74] A-Gonzalez N, Castrillo A (2018) Origin and specialization of splenic macrophages. Cell Immunol 330: 151-158. doi: 10.1016/j.cellimm.2018.05.005
    [75] Noelia A, Guillen JA, Gallardo G, et al. (2013) The nuclear receptor LXRα controls the functional specialization of splenic macrophages. Nat Immunol 14: 831. doi: 10.1038/ni.2622
    [76] McGaha TL, Chen Y, Ravishankar B, et al. (2011) Marginal zone macrophages suppress innate and adaptive immunity to apoptotic cells in the spleen. Blood 117: 5403-5412. doi: 10.1182/blood-2010-11-320028
    [77] van Dinther D, Veninga H, Iborra S, et al. (2018) Functional CD169 on macrophages mediates interaction with dendritic cells for CD8+ T cell cross-priming. Cell Rep 22: 1484-1495. doi: 10.1016/j.celrep.2018.01.021
    [78] Grabowska J, Lopez-Venegas MA, Affandi AJ, et al. (2018) CD169(+) macrophages capture and dendritic cells instruct: The interplay of the gatekeeper and the general of the immune system. Front Immunol 9: 2472-2472. doi: 10.3389/fimmu.2018.02472
    [79] Ravishankar B, Shinde R, Liu H, et al. (2014) Marginal zone CD169+ macrophages coordinate apoptotic cell-driven cellular recruitment and tolerance. Proc Natl Acad Sci USA 111: 4215-4220. doi: 10.1073/pnas.1320924111
    [80] Miyake Y, Asano K, Kaise H, et al. (2007) Critical role of macrophages in the marginal zone in the suppression of immune responses to apoptotic cell-associated antigens. J Clin Investig 117: 2268-2278. doi: 10.1172/JCI31990
    [81] Asano K, Nabeyama A, Miyake Y, et al. (2011) CD169-positive macrophages dominate antitumor immunity by crosspresenting dead cell-associated antigens. Immunity 34: 85-95. doi: 10.1016/j.immuni.2010.12.011
    [82] Prabagar MG, Do Y, Ryu S, et al. (2012) SIGN-R1, a C-type lectin, enhances apoptotic cell clearance through the complement deposition pathway by interacting with C1q in the spleen. Cell Death Differ 20: 535-545. doi: 10.1038/cdd.2012.160
    [83] Benoit ME, Clarke EV, Morgado P, et al. (2012) Complement protein C1q directs macrophage polarization and limits inflammasome activity during the uptake of apoptotic cells. J Immunol 188: 5682-5693. doi: 10.4049/jimmunol.1103760
    [84] Morelli AE (2003) Internalization of circulating apoptotic cells by splenic marginal zone dendritic cells: dependence on complement receptors and effect on cytokine production. Blood 101: 611-620. doi: 10.1182/blood-2002-06-1769
    [85] Morelli AE, Larregina AT, Shufesky WJ, et al. (2003) Internalization of circulating apoptotic cells by splenic marginal zone dendritic cells: dependence on complement receptors and effect on cytokine production. Blood 101: 611-620. doi: 10.1182/blood-2002-06-1769
    [86] Qiu CH, Miyake Y, Kaise H, et al. (2009) Novel subset of CD8α+ dendritic cells localized in the marginal zone is responsible for tolerance to cell-associated antigens. J Immunol 182: 4127-4136. doi: 10.4049/jimmunol.0803364
    [87] Yamazaki S, Dudziak D, Heidkamp GF, et al. (2008) CD8+ CD205+ splenic dendritic cells are specialized to induce Foxp3+ regulatory T cells. J Immunol 181: 6923-6933. doi: 10.4049/jimmunol.181.10.6923
    [88] Figgett WA, Fairfax K, Vincent FB, et al. (2013) The TACI receptor regulates T-cell-independent marginal zone B cell responses through innate activation-induced cell death. Immunity 39: 573-583. doi: 10.1016/j.immuni.2013.05.019
    [89] Ren W, Grimsholm O, Bernardi AI, et al. (2015) Surrogate light chain is required for central and peripheral B-cell tolerance and inhibits anti-DNA antibody production by marginal zone B cells. Eur J Immunol 45: 1228-1237. doi: 10.1002/eji.201444917
    [90] Sonoda KH, Stein-Streilein J (2002) CD1d on antigen-transporting APC and splenic marginal zone B cells promotes NKT cell-dependent tolerance. Eur J Immunol 32: 848-857. doi: 10.1002/1521-4141(200203)32:3<848::AID-IMMU848>3.0.CO;2-I
    [91] Miles K, Simpson J, Brown S, et al. (2018) Immune tolerance to apoptotic self is mediated primarily by regulatory B1a cells. Front Immunol 8: 1962. doi: 10.3389/fimmu.2017.01952
    [92] Kohyama M, Ise W, Edelson BT, et al. (2009) Role for Spi-C in the development of red pulp macrophages and splenic iron homeostasis. Nature 457: 318-321. doi: 10.1038/nature07472
    [93] Lin HH, Faunce DE, Stacey M, et al. (2005) The macrophage F4/80 receptor is required for the induction of antigen-specific efferent regulatory T cells in peripheral tolerance. J Exp Med 201: 1615-1625. doi: 10.1084/jem.20042307
    [94] Faunce DE, Stein-Streilein J (2002) NKT cell-derived RANTES recruits APCs and CD8+ T cells to the spleen during the generation of regulatory T cells in tolerance. J Immunol 169: 31-38. doi: 10.4049/jimmunol.169.1.31
    [95] Vendomèle J, Khebizi Q, Fisson S (2017) Cellular and molecular mechanisms of anterior chamber-associated immune deviation (ACAID): What we have learned from knockout mice. Front Immunol 8: 1686-1686. doi: 10.3389/fimmu.2017.01686
    [96] D'Orazio TJ, Niederkorn JY (1998) Splenic B cells are required for tolerogenic antigen presentation in the induction of anterior chamber-associated immune deviation (ACAID). Immunology 95: 47-55. doi: 10.1046/j.1365-2567.1998.00581.x
    [97] Ashour HM, Niederkorn JY (2006) Peripheral tolerance via the anterior chamber of the eye: role of B cells in MHC class I and II antigen presentation. J Immunol 176: 5950-5957. doi: 10.4049/jimmunol.176.10.5950
    [98] Vendomèle J, Dehmani S, Khebizi Q, et al. (2018) Subretinal injection of HY peptides induces systemic antigen-specific inhibition of effector CD4(+) and CD8(+) T-cell responses. Front Immunol 9: 504. doi: 10.3389/fimmu.2018.00504
    [99] Hos D, Schaub F, Cursiefen C (2019) Does anterior chamber-associated immune deviation (ACAID) play a role in posterior lamellar keratoplasty? Case report of a splenectomized patient. BMC Ophthalmol 19: 100. doi: 10.1186/s12886-019-1114-1
    [100] Cunnusamy K, Paunicka K, Reyes N, et al. (2010) Two different regulatory T cell populations that promote corneal allograft survival. Invest Ophth Vis Sci 51: 6566-6574. doi: 10.1167/iovs.10-6161
    [101] Kunishige T, Taniguchi H, Ohno T, et al. (2019) VISTA is crucial for corneal allograft survival and maintenance of immune privilege. Invest Ophth Vis Sci 60: 4958-4965. doi: 10.1167/iovs.19-27322
    [102] Koh AS, Miller EL, Buenrostro JD, et al. (2018) Rapid chromatin repression by Aire provides precise control of immune tolerance. Nat Immunol 19: 162-172. doi: 10.1038/s41590-017-0032-8
    [103] Gardner JM, DeVoss JJ, Friedman RS, et al. (2008) Deletional tolerance mediated by extrathymic Aire-expressing cells. Science 321: 843-847. doi: 10.1126/science.1159407
    [104] Gardner James M, Metzger Todd C, McMahon Eileen J, et al. (2013) Extrathymic Aire-expressing cells are a distinct bone marrow-derived population that induce functional inactivation of CD4+ T cells. Immunity 39: 560-572. doi: 10.1016/j.immuni.2013.08.005
    [105] Ravishankar B, Liu H, Shinde R, et al. (2012) Tolerance to apoptotic cells is regulated by indoleamine 2, 3-dioxygenase. P Natl Acad Sci USA 109: 3909-3914. doi: 10.1073/pnas.1117736109
    [106] Weiberg D, Basic M, Smoczek M, et al. (2018) Participation of the spleen in the IgA immune response in the gut. PLoS One 13: e0205247. doi: 10.1371/journal.pone.0205247
    [107] Edgar LJ, Kawasaki N, Nycholat CM, et al. (2018) Targeted delivery of antigen to activated CD169+ macrophages induces bias for expansion of CD8+ T cells. Cell Chem Biol 26: 131-136. doi: 10.1016/j.chembiol.2018.10.006
    [108] Sun LM, Chen HJ, Jeng LB, et al. (2015) Splenectomy and increased subsequent cancer risk: a nationwide population-based cohort study. Am J Surg 210: 243-251. doi: 10.1016/j.amjsurg.2015.01.017
    [109] Suzuki E, Kapoor V, Jassar AS, et al. (2005) Gemcitabine selectively eliminates splenic Gr-1+/CD11b+ myeloid suppressor cells in tumor-bearing animals and enhances antitumor immune activity. Clin Cancer Res 11: 6713-6721. doi: 10.1158/1078-0432.CCR-05-0883
    [110] Imai S, Nio Y, Shiraishi T, et al. (1991) Effects of splenectomy on pulmonary metastasis and growth of SC42 carcinoma transplanted into mouse liver. J Surg Oncol 47: 178-187. doi: 10.1002/jso.2930470309
    [111] Higashijima J, Shimada M, Chikakiyo M, et al. (2009) Effect of splenectomy on antitumor immune system in mice. Anticancer Res 29: 385-393.
    [112] Ge YG, Gao H, Kong XT (1989) Changes of peripheral T-cell subsets in asplenic W256 tumor-bearing rats. J Surg Oncol 42: 60-68. doi: 10.1002/jso.2930420113
    [113] Davis CJ, Ilstrup DM, Pemberton JH (1988) Influence of splenectomy on survival rate of patients with colorectal cancer. Am J Surg 155: 173-179. doi: 10.1016/S0002-9610(88)80276-9
    [114] Wanebo HJ, Kennedy BJ, Winchester DP, et al. (1997) Role of splenectomy in gastric cancer surgery: adverse effect of elective splenectomy on longterm survival. J Am Coll Surg 185: 177-184. doi: 10.1016/S1072-7515(01)00901-2
    [115] Fatouros M, Roukos DH, Lorenz M, et al. (2005) Impact of spleen preservation in patients with gastric cancer. Anticancer Res 25: 3023-3030.
    [116] Oh SJ, Hyung WJ, Li C, et al. (2009) The effect of spleen-preserving lymphadenectomy on surgical outcomes of locally advanced proximal gastric cancer. J Surg Oncol 99: 275-280. doi: 10.1002/jso.21229
    [117] Sonoda K, Izumi K, Matsui Y, et al. (2006) Decreased growth rate of lung metastatic lesions after splenectomy in mice. Eur Surg Res 38: 469-475. doi: 10.1159/000095415
    [118] Kossoy G, Ben-Hur H, Lifschitz O, et al. (2002) Mammary tumors in splenectomized rats. Oncol Rep 9: 185-188.
  • This article has been cited by:

    1. Zhen Zhang, Shance Wang, Relative subcategories with respect to a rigid subcategory, 2025, 0092-7872, 1, 10.1080/00927872.2025.2509823
  • Reader Comments
  • © 2021 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(15782) PDF downloads(1396) Cited by(33)

Figures and Tables

Figures(2)

/

DownLoad:  Full-Size Img  PowerPoint
Return
Return

Catalog