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人类免疫缺陷病毒(HIV)诱导的抗原特异性T细胞功能缺失是受主要组织相容性复合体(MHC)限制的。

HIV-induced deletion of antigen-specific T cell function is MHC restricted.

作者信息

Manca F, Newell A, Valle M, Habeshaw J, Dalgleish A G

机构信息

Department of Immunology, San Martino Hospital, University of Genoa, Italy.

出版信息

Clin Exp Immunol. 1992 Jan;87(1):15-9. doi: 10.1111/j.1365-2249.1992.tb06406.x.

DOI:10.1111/j.1365-2249.1992.tb06406.x
PMID:1733629
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1554242/
Abstract

When antigen-specific T cells are pulsed by antigen-presenting cells (APC) in the presence of HIV they are functionally deleted following subsequent exposure to syngeneic APC in the absence of HIV. Recombinant soluble HIV envelope (gp120) is able to induce a similar effect which, unlike that induced by HIV, is reversible. Neither HIV nor gp120 affect the ability to respond to IL-2. Thus it is only antigen-specific responses involving the T cell receptor pathways and CD4/MHC class II interaction that appear to be inhibited by HIV-1 and gp120. Furthermore, the functional impairment caused by HIV-1 is specific to the T cells that respond to the antigen in co-culture with HIV, as there is no apparent effect on 'bystander'-activated T cells specific for another antigen. Antigen-specific T cell lines may be deleted by a signalling mechanism which involves molecules other than gp120/CD4 but still requires MHC class II restriction.

摘要

当抗原特异性T细胞在存在HIV的情况下被抗原呈递细胞(APC)刺激时,随后在不存在HIV的情况下再次接触同基因APC后,它们会发生功能缺失。重组可溶性HIV包膜(gp120)能够诱导类似的效应,与HIV诱导的效应不同,这种效应是可逆的。HIV和gp120均不影响对IL-2的反应能力。因此,似乎只有涉及T细胞受体途径和CD4/II类主要组织相容性复合体相互作用的抗原特异性反应会受到HIV-1和gp120的抑制。此外,HIV-1导致的功能损伤特定于在与HIV共培养中对抗原产生反应的T细胞,因为对针对另一种抗原的“旁观者”激活的T细胞没有明显影响。抗原特异性T细胞系可能通过一种信号传导机制被清除,该机制涉及gp120/CD4以外的分子,但仍然需要II类主要组织相容性复合体限制。

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