期刊
JOURNAL OF NEUROIMMUNOLOGY
卷 106, 期 1-2, 页码 165-171出版社
ELSEVIER
DOI: 10.1016/S0165-5728(00)00238-1
关键词
experimental autoimmune encephalomyelitis; apoptosis; Fas; Bax
Recent studies have suggested that autoimmune inflammation elicited in the central nervous system (CNS) is subsided by apoptotic cell death of inflammatory cells. To elucidate the molecular mechanism of apoptosis of infiltrating T and other cells occurring in the CNS during autoimmune encephalomyelitis, we determined the type of apoptotic cells and the localization of apoptosis-related molecules (Fas, FasL, Bax, Bcl-2 and active caspase 3) by immunohistochemistry. Double labeling with the TUNEL method and cell-type markers showed that infiltrating T cells and microglia/macrophages underwent apoptosis, while astrocytes and neurons did not. Staining for apoptosis-related molecules revealed that infiltrating T cells and microglia/macrophages, but not astrocytes and neurons, expressed both Fas-FasL and Bax. The distribution and cell type of active caspase 3-positive cells were essentially the same as those of TUNEL-positive cells. These findings suggest that coexpression of Fas/FasL and Bax is closely associated with apoptotic cell death of infiltrating T cells and microglia in the CNS. Furthermore, astrocytes which express Fas and FasL, but not Bax, may play an important role in regulating inflammation in the CNS by inducing apoptotic cell death of infiltrating T cells and microglia, both of which have an inflammation-promoting nature. (C) 2000 Elsevier Science B.V. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据