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嗜T细胞的HIV gp120通过CXCR4介导CD4和CD8细胞趋化,与CD4无关:对HIV发病机制的启示。

T cell-tropic HIV gp120 mediates CD4 and CD8 cell chemotaxis through CXCR4 independent of CD4: implications for HIV pathogenesis.

作者信息

Iyengar S, Schwartz D H, Hildreth J E

机构信息

Department of Molecular Microbiology and Immunology, School of Hygiene Johns Hopkins University, Baltimore, MD 21205, USA.

出版信息

J Immunol. 1999 May 15;162(10):6263-7.

PMID:10229873
Abstract

HIV entry is determined by one or more chemokine receptors. T cell-tropic viruses bind CXCR4, whereas macrophage-tropic viruses use CCR5 and other CCRs. Infection with CXCR4 and CCR5-tropic HIV requires initial binding to CD4, and chemotaxis induced by the CCR5-tropic envelope has been reported to be strictly dependent on CD4 binding. We demonstrate that, in contrast to CD4-dependent gp120 signaling via CCR5, envelope signaling through CXCR4 is CD4 independent, inducing chemotaxis of both CD4 and CD8 T cells. Signaling by virus or soluble envelope through CXCR4 may affect pathogenesis by attracting and activating target and effector cells.

摘要

HIV的进入由一种或多种趋化因子受体决定。嗜T细胞病毒结合CXCR4,而嗜巨噬细胞病毒使用CCR5和其他CCR。感染CXCR4和CCR5嗜性的HIV需要首先结合CD4,并且据报道CCR5嗜性包膜诱导的趋化作用严格依赖于CD4结合。我们证明,与通过CCR5的CD4依赖性gp120信号传导相反,通过CXCR4的包膜信号传导不依赖于CD4,可诱导CD4和CD8 T细胞的趋化作用。病毒或可溶性包膜通过CXCR4发出的信号可能通过吸引和激活靶细胞和效应细胞来影响发病机制。

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