Suppr超能文献

在体外HIV-1感染时,Fas/FasL相互作用不参与活化的CD4+ T细胞的凋亡。

Fas/FasL interaction is not involved in apoptosis of activated CD4+ T cells upon HIV-1 infection in vitro.

作者信息

Yagi T, Sugimoto A, Tanaka M, Nagata S, Yasuda S, Yagita H, Kuriyama T, Takemori T, Tsunetsugu-Yokota Y

机构信息

Department of Immunology, AIDS Research Center, National Institute of Infectious Disease, Tokyo, Japan.

出版信息

J Acquir Immune Defic Syndr Hum Retrovirol. 1998 Aug 1;18(4):307-15. doi: 10.1097/00042560-199808010-00001.

Abstract

In HIV-1-infected individuals, Fas expression and Fas/FasL-mediated apoptosis of mature T cells are known to increase compared with those in normal individuals. To elucidate a relation between acute HIV-1 infection and the regulation of Fas/FasL system upon T-cell activation, resting CD4+ T cells were acutely infected or uninfected with HIV-1 and subsequently activated by phorbol myristate acetate and ionomycin (PMA/IM). Four days after infection, when HIV-1 env gp120 is expressed in more than one half of activated T cells, Fas/FasL expression was analyzed by flow cytometry, and apoptosis-inducing activity of these activated primary CD4+ T cells on Fas+ Jurkat cells was examined. The level of Fas or FasL expression was not altered during acute HIV-1 infection. The enhanced apoptosis-inducing activity upon HIV-1 infection was observed in some individuals, but its activity was not Fas/FasL-mediated. These results indicate that HIV-1 infection is not necessarily associated with either upregulation of Fas/FasL expression or Fas/FasL-mediated apoptosis.

摘要

在HIV-1感染个体中,与正常个体相比,已知成熟T细胞的Fas表达以及Fas/FasL介导的凋亡会增加。为了阐明急性HIV-1感染与T细胞激活后Fas/FasL系统调节之间的关系,将静息CD4+ T细胞急性感染HIV-1或不感染HIV-1,随后用佛波酯肉豆蔻酸酯乙酸盐和离子霉素(PMA/IM)激活。感染后四天,当超过一半的活化T细胞中表达HIV-1 env gp120时,通过流式细胞术分析Fas/FasL表达,并检测这些活化的原代CD4+ T细胞对Fas+ Jurkat细胞的凋亡诱导活性。在急性HIV-1感染期间,Fas或FasL表达水平未改变。在一些个体中观察到HIV-1感染后凋亡诱导活性增强,但其活性不是由Fas/FasL介导的。这些结果表明,HIV-1感染不一定与Fas/FasL表达上调或Fas/FasL介导的凋亡相关。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验