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本文引用的文献

1
MR1 presents microbial vitamin B metabolites to MAIT cells.MR1 将微生物维生素 B 代谢物呈递给 MAIT 细胞。
Nature. 2012 Nov 29;491(7426):717-23. doi: 10.1038/nature11605. Epub 2012 Oct 10.
2
Polyclonal mucosa-associated invariant T cells have unique innate functions in bacterial infection.多克隆黏膜相关不变 T 细胞在细菌感染中具有独特的先天功能。
Infect Immun. 2012 Sep;80(9):3256-67. doi: 10.1128/IAI.00279-12. Epub 2012 Jul 9.
3
Human thymic MR1-restricted MAIT cells are innate pathogen-reactive effectors that adapt following thymic egress.人类胸腺中受 MR1 限制的 MAIT 细胞是先天的病原体反应效应细胞,在离开胸腺后会进行适应性改变。
Mucosal Immunol. 2013 Jan;6(1):35-44. doi: 10.1038/mi.2012.45. Epub 2012 Jun 13.
4
Structural insight into MR1-mediated recognition of the mucosal associated invariant T cell receptor.MR1 介导的黏膜相关不变 T 细胞受体识别的结构见解。
J Exp Med. 2012 Apr 9;209(4):761-74. doi: 10.1084/jem.20112095. Epub 2012 Mar 12.
5
Innate IL-17 and IL-22 responses to enteric bacterial pathogens.先天免疫的 IL-17 和 IL-22 对肠道细菌病原体的反应。
Trends Immunol. 2012 Mar;33(3):112-8. doi: 10.1016/j.it.2012.01.003. Epub 2012 Feb 17.
6
Lymphoid tissue damage in HIV-1 infection depletes naïve T cells and limits T cell reconstitution after antiretroviral therapy.HIV-1 感染导致的淋巴组织损伤会消耗幼稚 T 细胞,并限制抗逆转录病毒治疗后 T 细胞的重建。
PLoS Pathog. 2012 Jan;8(1):e1002437. doi: 10.1371/journal.ppat.1002437. Epub 2012 Jan 5.
7
Microbial translocation across the GI tract.肠道微生物易位。
Annu Rev Immunol. 2012;30:149-73. doi: 10.1146/annurev-immunol-020711-075001. Epub 2012 Jan 3.
8
Human MAIT and CD8αα cells develop from a pool of type-17 precommitted CD8+ T cells.人类 MAIT 和 CD8αα 细胞来源于 17 型先天预定向 CD8+T 细胞池。
Blood. 2012 Jan 12;119(2):422-33. doi: 10.1182/blood-2011-05-353789. Epub 2011 Nov 15.
9
Induction of lectin-like transcript 1 (LLT1) protein cell surface expression by pathogens and interferon-γ contributes to modulate immune responses.病原体和干扰素-γ诱导凝集素样转录本 1(LLT1)蛋白的细胞表面表达,有助于调节免疫反应。
J Biol Chem. 2011 Nov 4;286(44):37964-37975. doi: 10.1074/jbc.M111.285312. Epub 2011 Sep 19.
10
Mucosal-associated invariant T cells regulate Th1 response in multiple sclerosis.黏膜相关恒定 T 细胞调节多发性硬化症中的 Th1 反应。
Int Immunol. 2011 Sep;23(9):529-35. doi: 10.1093/intimm/dxr047. Epub 2011 Jun 28.

慢性 HIV-1 感染中抗菌性 MR1 限制性 MAIT 细胞群体的激活、耗竭和持续衰退。

Activation, exhaustion, and persistent decline of the antimicrobial MR1-restricted MAIT-cell population in chronic HIV-1 infection.

机构信息

Center for Infectious Medicine, Department of Medicine, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden.

出版信息

Blood. 2013 Feb 14;121(7):1124-35. doi: 10.1182/blood-2012-07-445429. Epub 2012 Dec 13.

DOI:10.1182/blood-2012-07-445429
PMID:23243281
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3575756/
Abstract

Mucosal-associated invariant T (MAIT) cells are an evolutionarily conserved antimicrobial MR1-restricted T-cell subset. MAIT cells are CD161(+), express a V7.2 TCR, are primarily CD8(+) and numerous in blood and mucosal tissues. However, their role in HIV-1 infection is unknown. In this study, we found levels of MAIT cells to be severely reduced in circulation in patients with chronic HIV-1 infection. Residual MAIT cells were highly activated and functionally exhausted. Their decline was associated with time since diagnosis, activation levels, and the concomitant expansion of a subset of functionally impaired CD161(+) V7.2(+) T cells. Such cells were generated in vitro by exposure of MAIT cells to Escherichia coli. Notably, whereas the function of residual MAIT cells was at least partly restored by effective antiretroviral therapy, levels of MAIT cells in peripheral blood were not restored. Interestingly, MAIT cells in rectal mucosa were relatively preserved, although some of the changes seen in blood were recapitulated in the mucosa. These findings are consistent with a model in which the MAIT-cell compartment, possibly as a result of persistent exposure to microbial material, is engaged, activated, exhausted, and progressively and persistently depleted during chronic HIV-1 infection.

摘要

黏膜相关恒定 T(MAIT)细胞是一种进化上保守的、受 MR1 限制的抗微生物的 T 细胞亚群。MAIT 细胞表达 CD161(+)、V7.2TCR,主要为 CD8(+),在血液和黏膜组织中数量众多。然而,它们在 HIV-1 感染中的作用尚不清楚。在这项研究中,我们发现慢性 HIV-1 感染患者的循环中 MAIT 细胞水平严重降低。残留的 MAIT 细胞高度活化并功能耗竭。它们的减少与诊断后的时间、激活水平以及功能受损的 CD161(+)V7.2(+)T 细胞亚群的同时扩张有关。这些细胞在体外通过 MAIT 细胞暴露于大肠杆菌而产生。值得注意的是,尽管有效的抗逆转录病毒疗法至少部分恢复了残留 MAIT 细胞的功能,但外周血中的 MAIT 细胞水平并未恢复。有趣的是,直肠黏膜中的 MAIT 细胞相对保存,尽管在血液中观察到的一些变化在黏膜中得到了重现。这些发现与 MAIT 细胞区室可能由于持续暴露于微生物物质而被激活、耗竭并在慢性 HIV-1 感染过程中逐渐和持续消耗的模型一致。