CD95信号不是下调对系统性结核分枝杆菌感染的细胞反应所必需的

J.E. Pearl, I.M. Orme, A.M. Cooper
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引用次数: 4

摘要

结核患者对分枝杆菌抗原的细胞反应有降低的趋势,这种减少与CD4 T细胞的凋亡有关。为了确定CD95在介导结核病抗原特异性淋巴细胞凋亡中的作用,我们将CD95L分子突变的小鼠全身感染致病性结核分枝杆菌。对照小鼠和CD95L突变小鼠都表现出预期的对分枝杆菌抗原的反应丧失,唯一的区别是突变小鼠的反应丧失略有延迟。突变小鼠反应的有限持久性表明,虽然感染分枝杆菌的小鼠的抗原特异性细胞反应确实下降,但这种下降并不依赖于CD95L。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
CD95 signaling is not required for the down regulation of cellular responses to systemic Mycobacterium tuberculosis infection

There is a tendency among tuberculosis patients to have reduced cellular responses to mycobacterial antigens and this loss has been associated with apoptosis of CD4 T cells. In order to determine the role of CD95 in mediating apoptosis of antigen-specific lymphocytes in tuberculosis, mice with a mutated CD95L molecule were infected systemically with virulent Mycobacterium tuberculosis. Both control and CD95L mutant mice exhibited the expected loss of response to mycobacterial antigens, with the only difference being a slight delay in the loss of the response in the mutant mice. The limited persistence of the response in the mutant mice suggests that, while antigen-specific cellular responses do decline in mice infected with mycobacteria, this decline is not dependent upon CD95L.

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