Homeostatic expansion of T cells during immune insufficiency generates autoimmunity
Homeostatic expansion of T cells during immune insufficiency generates autoimmunity
复制标题
DOI：
10.1016/s0092-8674(04)00335-6
复制
发表时间：
2004-04-16
期刊：
影响因子：
64.5
通讯作者：
Sarvetnick, N
中科院分区：
文献类型：
--
作者：
King, C;Ilic, A;Sarvetnick, N
在疾病和压力期间，免疫系统会遭受相当大的T细胞损失（淋巴细胞减少）。剩下的T细胞经历剧烈的代偿性扩张，称为稳态增殖，以重建免疫系统。有趣的是，人类自身免疫性疾病通常表现为免疫缺陷，如淋巴细胞减少症。在这项研究中，我们表明减少T细胞数量和由此产生的夸大稳态型T细胞增殖产生自身免疫。循环的T细胞群寿命很短，耗尽的记忆区为新的效应T细胞的产生提供燃料。这些现象的催化剂是对细胞因子IL-21的反应增加，IL-21是调节T细胞周转的介质。我们的结论是，T细胞存活率低和淋巴细胞减少导致自身免疫性疾病。
During illness and stress, the immune system can suffer a considerable loss of T cells (lymphopenia). The remaining T cells undergo vigorous compensatory expansion, known as homeostatic proliferation, to reconstitute the immune system. Interestingly, human diseases of autoimmune etiology often present with immune deficiencies such as lymphopenia. In this study, we show that reduced T cell numbers and the resulting exaggerated homeostatic-type proliferation of T cells generate autoimmunity. The cycling T cell population is short lived, and the depleted memory compartment fuels the generation of new effector T cells. A catalyst for these phenomena is the increased responses to the cytokine IL-21, a mediator that regulates T cell turnover. We conclude that poor T cell survival and lymphopenia precipitate autoimmune disease.