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小鼠逆转录病毒诱导的免疫缺陷综合征中派尔集合淋巴结淋巴细胞通过CD95(Fas)依赖性和非依赖性机制发生的细胞凋亡

Apoptosis by CD95 (Fas)-dependent and -independent mechanisms in Peyer's patch lymphocytes in murine retrovirus-induced immunodeficiency syndrome.

作者信息

Usami J, Hiromatsu K, Aoki Y, Kobayashi N, Makino M, Yagita H, Matsumoto Y, Maeda K, Yoshikai Y

机构信息

Department of Internal Medicine, Nagoya University Branch Hospital, Japan.

出版信息

J Virol. 1996 Dec;70(12):8917-25. doi: 10.1128/JVI.70.12.8917-8925.1996.

Abstract

CD95 (Fas)/CD95 ligand (CD95 L)-mediated apoptosis is thought to be involved in the delayed progression of murine AIDS (MAIDS) induced by LP-BM5 murine leukemia virus (MuLV). We show evidence of apoptosis in lymphocytes of Peyer's patches (PP) at the early stage of MAIDS. Both T and B cells in PP expressed CD95 at the early stage of MAIDS and decreased in number thereafter. The decrease in T cells was not evident in CD95-mutated lpr mice with MAIDS, suggesting that CD95/CD95 L interaction is involved in the apoptosis of T cells in PP during the course of MAIDS. On the other hand, the number of B cells was also decreased in PP of lpr mice with MAIDS. The proliferative ability of B cells in PP of MAIDS mice in response to immunoglobulin M cross-linking or lipopolysaccharide was severely impaired, while the B cells normally proliferated in response to anti-CD40 monoclonal antibody. These findings imply that aberrantly activated B cells in PP undergo apoptosis independently of the CD95/CD95 L system during the course of infection with MAIDS virus.

摘要

CD95(Fas)/CD95配体(CD95L)介导的细胞凋亡被认为与LP - BM5小鼠白血病病毒(MuLV)诱导的小鼠获得性免疫缺陷综合征(MAIDS)的延迟进展有关。我们展示了在MAIDS早期派尔集合淋巴结(PP)淋巴细胞中存在细胞凋亡的证据。在MAIDS早期,PP中的T细胞和B细胞均表达CD95,此后数量减少。在患有MAIDS的CD95突变型lpr小鼠中,T细胞数量的减少并不明显,这表明在MAIDS病程中,CD95/CD95L相互作用参与了PP中T细胞的凋亡。另一方面,患有MAIDS的lpr小鼠PP中的B细胞数量也减少。MAIDS小鼠PP中B细胞对免疫球蛋白M交联或脂多糖的增殖能力严重受损,而B细胞对抗CD40单克隆抗体通常会正常增殖。这些发现意味着在感染MAIDS病毒的过程中,PP中异常激活的B细胞独立于CD95/CD95L系统发生凋亡。

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