T-cell apoptosis in inflammatory brain lesions - Destruction of T cells does not depend on antigen recognition
T-cell apoptosis in inflammatory brain lesions - Destruction of T cells does not depend on antigen recognition
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DOI：
10.1016/s0002-9440(10)65615-5
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发表时间：
1998-09-01
影响因子：
6
通讯作者：
Lassmann, H
中科院分区：
文献类型：
--
作者：
Bauer, J;Bradl, M;Lassmann, H
通过细胞凋亡消除炎性T细胞似乎在中枢神经系统炎症的下调中起着重要作用。在此，我们报告了在不同的自身免疫性脑脊髓炎模型中，T淋巴细胞发生类似程度的凋亡。细胞凋亡仅限于神经外胚层实质中的细胞，从而使存在于大脑结缔组织隔室中的T细胞不受损害。实质内T细胞的死亡不依赖于常驻的小胶质细胞或星形胶质细胞的抗原提呈。携带特定遗传标记的T淋巴细胞过继转移实验显示，在中枢神经系统中，无论其抗原特异性或激活状态如何，这些细胞都会被摧毁。虽然许多抗原依赖和非抗原依赖的诱导T细胞凋亡的机制可能同时起作用，但我们的结果表明，神经系统具有一种特殊的、目前尚未确定的机制，可以有效地消除浸润性T淋巴细胞。
Elimination of inflammatory T cells by apoptosis appears to play an important role in the down-regulation of inflammation in the central nervous system. Here we report that apoptosis of T lymphocytes occurs to a similar extent in different models of auto immune encephalomyelitis. Apoptosis is restricted to cells located in the neuroectodermal parenchyma, thereby leaving T cells present in the brain's connective tissue compartments unharmed. Death of T cells in the parenchyma does not depend on antigen presentation by resident microglial cells or astrocytes. Adoptive transfer experiments with T lymphocytes carrying a specific genetic marker revealed that in the central nervous system these cells are destroyed regardless of their antigen specificity or state of activation. Although many of both antigen-dependent and -independent mechanisms in the induction of T-cell apoptosis may act simultaneously, our results suggest that the nervous system harbors a specific, currently undefined, mechanism that effectively eliminates infiltrating T lymphocytes.