T cell immunity in autoimmune hepatitis
T cell immunity in autoimmune hepatitis
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DOI：
10.1016/j.autrev.2005.01.005
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发表时间：
2005-06-01
影响因子：
13.6
通讯作者：
Gershwin, ME
中科院分区：
文献类型：
--
作者：
Ichiki, Y;Aoki, CA;Gershwin, ME
T 细胞在 AM 的免疫发病机制中发挥核心作用。直到最近，CD4(+) T 细胞还被认为对疾病的发展至关重要，越来越多的证据表明 CD8(+) T 和 γ δ T 细胞也发挥着重要作用。某些 HLA 基因型对 AM 的易感性以及有限数量的 T 细胞受体的克隆扩增表明自身抗原或分子模拟物的呈现可能是免疫反应启动的原因。鉴于AIH与病毒性肝炎的关联，人们认为耐受性的丧失始于肝细胞的感染以及随后的CD8+T细胞的细胞溶解。自身抗原或分子模拟物的呈现导致 T 细胞的激活和克隆扩增；调节性 T 细胞受损和细胞凋亡缺陷可能会加剧这一过程。最终，T 细胞启动 B 细胞产生自身抗体、促炎细胞因子，最后产生肝细胞的细胞毒性。 (c) 2005 Elsevier B.V. 保留所有权利。
T cells play a central role in the immunopathogenesis of AM. Until recently CD4(+) T cells were thought to be critical for disease development, increasing evidence has shown that CD8(+) T and gamma delta T cells also play a significant role. The predisposition of certain HLA genotypes to AM as well as the clonal expansion of a limited number of T cell receptors suggests that the presentation of a self-antigen or a molecular mimic may be responsible for the initiation of the immune response. Given the association of AIH with viral hepatitis, it is thought that the loss of tolerance begins with an infection of hepatocytes and subsequent cytolysis by CD8(+) T cells. The presentation of self-antigens or molecular mimics leads to activation and clonal expansion of T cells; this process may be increased by impaired regulatory T cells and a defect in apoptosis. Ultimately T cells initiate B cell production of autoantibodies, proinflammatory cytokines and finally hepatocyte cytotoxicity. (c) 2005 Elsevier B.V. All rights reserved.