Activation pathways that drive CD4(+) T cells to break tolerance in autoimmune diseases().
Activation pathways that drive CD4(+) T cells to break tolerance in autoimmune diseases().
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DOI：
10.1111/imr.13071
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发表时间：
2022-05
影响因子：
8.7
通讯作者：
中科院分区：
文献类型：
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作者：
自身免疫性疾病的特征是免疫系统功能失调，将自我误认为非自我并导致组织破坏。几种细胞类型与引发和维持疾病有关。由于主要组织相容性复合体II（MHC-II）蛋白与各种自身免疫性疾病的强关联，CD 4 + T淋巴细胞已被彻底研究其在决定疾病过程中的作用。CD 4 + T细胞活化是一个协调的过程，需要三种不同的信号：信号1，由MHC-II分子上的抗原识别介导;信号2，以共刺激方式增强信号1;信号3，有助于将活化的细胞分化为功能相关的亚群。这些信号在自身免疫过程中被破坏，并促使CD 4 + T细胞破坏耐受性。在此，我们回顾了我们目前对这三种信号中的每一种在三种不同的自身免疫性疾病中发挥作用的理解，并强调了使个体易患自身免疫性疾病的遗传多态性。我们还讨论了现有疗法的缺点，以及如何解决这些问题以实现患者的持久耐受。
Autoimmune diseases are characterized by dysfunctional immune systems that misrecognize self as non-self and cause tissue destruction. Several cell types have been implicated in triggering and sustaining disease. Due to a strong association of major histocompatibility complex II (MHC-II) proteins with various autoimmune diseases, CD4+ T lymphocytes have been thoroughly investigated for their roles in dictating disease course. CD4+ T cell activation is a coordinated process that requires three distinct signals: Signal 1, which is mediated by antigen recognition on MHC-II molecules; Signal 2, which boosts signal 1 in a costimulatory manner; and Signal 3, which helps to differentiate the activated cells into functionally relevant subsets. These signals are disrupted during autoimmunity and prompt CD4+ T cells to break tolerance. Herein, we review our current understanding of how each of the three signals plays a role in three different autoimmune diseases and highlight the genetic polymorphisms that predispose individuals to autoimmunity. We also discuss the drawbacks of existing therapies and how they can be addressed to achieve lasting tolerance in patients.
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影响因子：
30.8
作者：
Barrett, Jeffrey C.;Clayton, David G.;Concannon, Patrick;Akolkar, Beena;Cooper, Jason D.;Erlich, Henry A.;Julier, Cecile;Morahan, Grant;Nerup, Jorn;Nierras, Concepcion;Plagnol, Vincent;Pociot, Flemming;Schuilenburg, Helen;Smyth, Deborah J.;Stevens, Helen;Todd, John A.;Walker, Neil M.;Rich, Stephen S.
通讯作者：
Rich, Stephen S.
DOI：
10.1126/science.1198469
发表时间：
2011-01-21
期刊：
Science (New York, N.Y.)
影响因子：
--
作者：
Atarashi K;Tanoue T;Shima T;Imaoka A;Kuwahara T;Momose Y;Cheng G;Yamasaki S;Saito T;Ohba Y;Taniguchi T;Takeda K;Hori S;Ivanov II;Umesaki Y;Itoh K;Honda K
通讯作者：
Honda K
影响因子：
82.9
作者：
通讯作者：
--
DOI：
10.4049/jimmunol.1301480
发表时间：
2013-10-15
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Baker RL;Delong T;Barbour G;Bradley B;Nakayama M;Haskins K
通讯作者：
Haskins K
影响因子：
4.8
作者：
Aggarwal, S;Ghilardi, N;Gurney, AL
通讯作者：
Gurney, AL