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本文引用的文献

1
Small molecule inhibition of HIV-1-induced MHC-I down-regulation identifies a temporally regulated switch in Nef action.小分子抑制 HIV-1 诱导的 MHC-I 下调,确定了 Nef 作用中的一个时间调节开关。
Mol Biol Cell. 2010 Oct 1;21(19):3279-92. doi: 10.1091/mbc.E10-05-0470. Epub 2010 Aug 11.
2
Immune evasion and counteraction of restriction factors by HIV-1 and other primate lentiviruses.HIV-1 和其他灵长类慢病毒的免疫逃逸和对限制因子的拮抗作用。
Cell Host Microbe. 2010 Jul 22;8(1):55-67. doi: 10.1016/j.chom.2010.06.004.
3
HIV-1 Nef binds a subpopulation of MHC-I throughout its trafficking itinerary and down-regulates MHC-I by perturbing both anterograde and retrograde trafficking.HIV-1 Nef 在其整个运输途径中结合 MHC-I 的一个亚群,并通过扰乱正向和逆向运输来下调 MHC-I。
J Biol Chem. 2010 Oct 1;285(40):30884-905. doi: 10.1074/jbc.M110.135947. Epub 2010 Jul 9.
4
The great escape: viral strategies to counter BST-2/tetherin.大逃亡:病毒对抗 BST-2/ tetherin 的策略。
PLoS Pathog. 2010 May 13;6(5):e1000913. doi: 10.1371/journal.ppat.1000913.
5
In vivo CD8+ T-cell suppression of siv viremia is not mediated by CTL clearance of productively infected cells.体内 CD8+ T 细胞对 SIV 病毒血症的抑制作用不是由 CTL 清除感染细胞引起的。
PLoS Pathog. 2010 Jan 29;6(1):e1000748. doi: 10.1371/journal.ppat.1000748.
6
An MHC-I cytoplasmic domain/HIV-1 Nef fusion protein binds directly to the mu subunit of the AP-1 endosomal coat complex.一种 MHC-I 胞质结构域/ HIV-1 Nef 融合蛋白直接结合到 AP-1 内体衣被复合物的 μ 亚基上。
PLoS One. 2009 Dec 18;4(12):e8364. doi: 10.1371/journal.pone.0008364.
7
At the crossroads of homoeostasis and disease: roles of the PACS proteins in membrane traffic and apoptosis.在稳态与疾病的交叉点:PACS蛋白在膜运输和细胞凋亡中的作用
Biochem J. 2009 Jun 12;421(1):1-15. doi: 10.1042/BJ20081016.
8
MHC class I antigen presentation: learning from viral evasion strategies.MHC I类抗原呈递:从病毒逃逸策略中学习
Nat Rev Immunol. 2009 Jul;9(7):503-13. doi: 10.1038/nri2575.
9
A structural explanation for the binding of endocytic dileucine motifs by the AP2 complex.AP2复合物结合内吞双亮氨酸基序的结构解释。
Nature. 2008 Dec 18;456(7224):976-979. doi: 10.1038/nature07422.
10
HIV-1 Nef targets MHC-I and CD4 for degradation via a final common beta-COP-dependent pathway in T cells.HIV-1 Nef通过T细胞中一条最终共同的依赖β-COP的途径靶向MHC-I和CD4进行降解。
PLoS Pathog. 2008 Aug 22;4(8):e1000131. doi: 10.1371/journal.ppat.1000131.

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.

DOI:10.1016/B978-0-12-385987-7.00005-1
PMID:21762823
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3782996/
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。