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HIV 免疫逃逸:HIV Nef 蛋白对抗原呈递的干扰。

HIV immune evasion disruption of antigen presentation by the HIV Nef protein.

机构信息

Graduate Program in Cellular and Molecular Biology, University of Michigan, Ann Arbor, Michigan, USA.

出版信息

Adv Virus Res. 2011;80:103-27. doi: 10.1016/B978-0-12-385987-7.00005-1.

Abstract

The Human Immunodeficiency Virus (HIV) Nef protein is necessary for high viral loads and for timely progression to AIDS. Nef plays a number of roles, but its effect on antigen presentation and immune evasion are among the best characterized. Cytotoxic T lymphocytes (CTLs) recognize and lyse virally infected cells by detecting viral antigens in complex with host major histocompatibility complex class I (MHC-I) molecules on the infected cell surface. The HIV Nef protein disrupts antigen presentation at the cell surface by interfering with the normal trafficking pathway of MHC-I and thus reduces CTL recognition and lysis of infected cells. The molecular mechanism by which Nef causes MHC-I downmodulation is becoming more clear, but some questions remain. A better understanding of how Nef disrupts antigen presentation may lead to the development of drugs that enhance the ability of the anti-HIV CTLs to control HIV disease.

摘要

人类免疫缺陷病毒 (HIV) 的 Nef 蛋白对于高病毒载量和及时进展为艾滋病是必要的。Nef 发挥了多种作用,但它对抗原呈递和免疫逃逸的影响是最具特征的。细胞毒性 T 淋巴细胞 (CTL) 通过识别病毒感染细胞表面与宿主主要组织相容性复合体 I 类 (MHC-I) 分子结合的病毒抗原,来识别和裂解病毒感染的细胞。HIV Nef 蛋白通过干扰 MHC-I 的正常运输途径,在细胞表面破坏抗原呈递,从而减少 CTL 对感染细胞的识别和裂解。Nef 导致 MHC-I 下调的分子机制变得越来越清晰,但仍存在一些问题。更好地了解 Nef 如何破坏抗原呈递,可能会导致开发出增强抗 HIV CTL 控制 HIV 疾病能力的药物。

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