一項(xiàng)研究發(fā)現(xiàn)，那些可以抵抗艾滋病毒的人，體內(nèi)所含的一種基因令他們擁有一個更加強(qiáng)大的免疫系統(tǒng)。

研究發(fā)現(xiàn)，有一小部分人（大約每200名感染者中就有這樣一個人）接觸艾滋病毒后，發(fā)展成艾滋病的速度很慢，甚至不會患上這種致命疾病。以前的研究發(fā)現(xiàn)，很多天生具有艾滋病毒免疫能力的人，體內(nèi)含有一種被稱作HLA B57的基因。

在這項(xiàng)研究中美國研究人員發(fā)現(xiàn)，HLA B57促使身體產(chǎn)生更多強(qiáng)大的殺傷T細(xì)胞。殺傷T細(xì)胞是會對具有感染性的入侵者發(fā)起攻擊的白細(xì)胞。與沒有這種基因的人相比，那些擁有HLA B57的人體內(nèi)含有大量可以束縛住艾滋病毒蛋白的T細(xì)胞。擁有HLA B57的人，體內(nèi)的T細(xì)胞更有可能識別出代表艾滋病毒蛋白的細(xì)胞，其中包括在感染過程中產(chǎn)生的變異蛋白。

據(jù)馬薩諸塞州總醫(yī)院拉貢研究所、麻省理工學(xué)院和哈佛大學(xué)的研究人員說，這些發(fā)現(xiàn)或許有助于科學(xué)家研發(fā)出艾滋病疫苗，它引起的免疫響應(yīng)，與具有HLA B57基因的人對艾滋病毒做出的免疫響應(yīng)

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Effects of thymic selection of the T-cell repertoire on HLA classI-associated
 control of HIV infection
Andrej Kosmrlj ^1,2,9, Elizabeth L. Read ^1,3,4,9, Ying Qi5, Todd M. Allen ¹, Marcus Altfeld ^1,
Steven G. Deeks ⁶, Florencia Pereyra ^1, Mary Carrington ^1,5,
Bruce D. Walker ^1,7 & Arup K. Chakraborty ^1,3,4,8

1.Ragon Institute of MGH, MIT and Harvard, Boston, Massachusetts 02114, USA
2.Department of Physics, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA
3.Department of Chemical Engineering, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA
4.Department of Chemistry, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA
5.Cancer and Inflammation Program, Laboratory of Experimental Immunology, SAIC-Frederick, Inc., NCI-Frederick, Frederick, Maryland 21702, USA
6.University of California, San Francisco, California 94110, USA
7.Howard Hughes Medical Institute, Chevy Chase, Maryland 20815, USA
8.Department of Biological Engineering, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA
9.These authors contributed equally to this work.

【Abstract】Without therapy, most people infected with human immunodeficiency virus （HIV） ultimay progress to AIDS. Rare individuals （‘elite controllers’） maintain very low levels of HIV RNA without therapy, thereby making disease progression and transmission unlikely. Certain HLA class I alleles are markedly enriched in elite controllers, with the highest association observed for HLA-B57 （ref. 1）. Because HLA molecules present viral peptides that activate CD8+ T cells, an immune-mediated mechanism is probably responsible for superior control of HIV. Here we describe how the peptide-binding characteristics of HLA-B57 molecules affect thymic development such that, compared to other HLA-restricted T cells, a larger fraction of the naive repertoire of B57-restricted clones recognizes a viral epitope, and these T cells are more cross-reactive to mutants of targeted epitopes. Our calculations predict that such a T-cell repertoire imposes strong immune pressure on immunodominant HIV epitopes and emergent mutants, thereby promoting efficient control of the virus. Supporting these predictions, in a large cohort of HLA-typed individuals, our experiments show that the relative ability of HLA-B alleles to control HIV correlates with their peptide-binding characteristics that affect thymic development. Our results provide a conceptual framework that unifies diverse empirical observations, and have implications for vaccination strategies.