Tumor necrosis factor receptor p55 mediates deletion of peripheral cytotoxic T lymphocytes in vivo
Tumor necrosis factor receptor p55 mediates deletion of peripheral cytotoxic T lymphocytes in vivo
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DOI：
10.1002/eji.1830261235
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发表时间：
1996-12-01
影响因子：
5.4
通讯作者：
Ohashi, PS
中科院分区：
文献类型：
--
作者：
Speiser, DE;Sebzda, E;Ohashi, PS
活化淋巴细胞的细胞死亡下调免疫应答，并参与维持自身耐受。与膜分子Fas的连接相关的信号导致淋巴细胞凋亡，但是已经假定了另外的Fas非依赖性机制。在这里，我们显示了一个显着的扩展和持久的功能激活的细胞毒性T细胞在小鼠缺乏肿瘤坏死因子（TNF）受体p55。在缺乏该受体的情况下，体内外周淋巴细胞凋亡显着减少。胸腺细胞存活时间延长与功能性无能有关，因为T细胞在体外用肽抗原刺激时不再增殖。然而，特异性细胞毒性效应子功能在体外很容易检测到。我们的结论是，TNF受体p55参与外周T细胞在体内的删除。
Cellular death of activated lymphocytes down-regulates immune responses and is involved in maintaining self tolerance. Signals associated with ligation of the membrane molecule Fas lead to lymphocyte apoptosis, but additional, Fas-independent mechanisms have been postulated. Here, we show a marked expansion and prolonged persistence of functional activated cytotoxic T cells in mice lacking the tumor necrosis factor (TNF) receptor p55. In the absence of this receptor, peripheral lymphocyte apoptosis was significantly reduced in vivo. The prolonged thymocyte survival was associated with functional anergy, since the T cells no longer proliferated in vitro when stimulated with peptide antigen. However, specific cytotoxic effector function was easily detected in vitro. We conclude that the TNF receptor p55 is involved in peripheral T cell deletion in vivo.