The relationship of inflammation and initiation of autoimmune disease: role of TNF super family members.
The relationship of inflammation and initiation of autoimmune disease: role of TNF super family members.
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DOI：
10.1007/978-3-662-04700-2_1
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发表时间：
2002
影响因子：
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通讯作者：
R. Flavell
中科院分区：
文献类型：
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作者：
R. Flavell
在正常人中，在通过宿主抗原呈递细胞（APC）将自身肽呈递给自身反应性T细胞之后，自身反应性T细胞可以在胸腺或外周中被删除（KuRTS等）。1996，1998 a，B）。据信，这种假定的耐受机制的崩溃会导致遗传易感个体的自身免疫性。I型糖尿病是以免疫细胞浸润胰岛为特征，通过T细胞介导的机制最终破坏胰岛素产生细胞。这种自身免疫的T细胞介导的性质要求APC不仅必须呈递从~-细胞释放的胰岛抗原，而且必须传递促进自身活性T细胞存活的信号。识别启动和维持这种抗胰岛炎症反应的细胞和事件对于开发糖尿病治疗策略至关重要。
In normal people, autoreactive T cells can be deleted, either in the thymus or in the periphery, following presentation of self-peptides by host antigenpresenting cells (APCs) to self-reactive T cells (KuRTS eta!. 1996, 1998a, b). Breakdown in this putative tolerance mechanism is believed to contribute to autoimmunity in genetically susceptible individuals. Type I diabetes mellitus is characterized by infiltration of the islets of Langerhans by immune cells, which ultimately destroy the insulin-producing~-cells by T cellmediated mechanisms. The T cell-mediated nature of this autoimmunity requires that APCs not only have to present islet antigen released from~-cells but also have to deliver signals that promote survival of the selfreactive T cells. Identification of the cells and events that initiate and maintain this anti-islet inflammatory response is vital in the development of therapeutic strategies towards diabetes.