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HIV-1感染中的HLA-I类特异性抑制性受体

HLA-class I-specific inhibitory receptors in HIV-1 infection.

作者信息

De Maria A, Moretta L

机构信息

Department of Internal Medicine, University of Genova, Italy.

出版信息

Hum Immunol. 2000 Jan;61(1):74-81. doi: 10.1016/s0198-8859(99)00169-x.

Abstract

One of the most characteristic and, at the same time, puzzling features of the cellular immune response towards HIV-1 is represented by an early vigorous HIV-specific CD8+ CTL response that does not prevent disease progression in the vast majority of patients. In this context, there is a striking mismatch over the course of disease progression between increasing numbers of activated CD8+ T cells and apparent decrease of virus-specific CD8+ CTLs. Inhibitory NK receptors (iNKRs) specific for HLA class I molecules can be expressed on CD8+ T-cells of healthy individuals and deliver inhibitory signals that determine decreased CTL function. Their expression on CD8+ CTL may be induced by IL-15 or TGFP in vitro, and may represent an important regulatory function for the fine-tuning of the antigen-specific T cell response against tumors and intracytoplasmic pathogens. In HIV-1 infected patients, relevant proportions of peripheral blood CD8+ T lymphocytes express iNKRs belonging to the Ig superfamily (p58/p70/p140) and CD94/NKG2A. Presence of iNKRs on CD8+ CTLs impairs HIV-1-specific cytolytic activity in vitro and may allow uncontrolled viral replication and spread following functional inhibition of CTL effectors in infected patients.

摘要

细胞免疫对HIV-1反应的最典型且同时令人困惑的特征之一,表现为早期强烈的HIV特异性CD8+CTL反应,而在绝大多数患者中这种反应并不能阻止疾病进展。在此背景下,在疾病进展过程中,活化的CD8+T细胞数量不断增加与病毒特异性CD8+CTL明显减少之间存在显著不匹配。对HLA I类分子特异的抑制性NK受体(iNKRs)可在健康个体的CD8+T细胞上表达,并传递决定CTL功能降低的抑制性信号。它们在CD8+CTL上的表达在体外可由IL-15或转化生长因子β(TGFβ)诱导,并且可能代表针对肿瘤和胞浆内病原体的抗原特异性T细胞反应进行微调的重要调节功能。在HIV-1感染患者中,外周血CD8+T淋巴细胞的相关比例表达属于Ig超家族的iNKRs(p58/p70/p140)和CD94/NKG2A。CD8+CTL上存在iNKRs会损害体外HIV-1特异性细胞溶解活性,并可能在感染患者中CTL效应器功能受到抑制后导致病毒不受控制地复制和传播。

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