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DOI | 10.1126/science.aam8825 |
Elevated HLA-A expression impairs HIV control through inhibition of NKG2A-expressing cells | |
Ramsuran, Veron1; 39;u, Thumbi2 | |
2018-01-05 | |
发表期刊 | SCIENCE
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ISSN | 0036-8075 |
EISSN | 1095-9203 |
出版年 | 2018 |
卷号 | 359期号:6371页码:86-90 |
文章类型 | Article |
语种 | 英语 |
国家 | USA; South Africa; England; Switzerland; Germany |
英文摘要 | The highly polymorphic human leukocyte antigen (HLA) locus encodes cell surface proteins that are critical for immunity. HLA-A expression levels vary in an allele-dependent manner, diversifying allele-specific effects beyond peptide-binding preference. Analysis of 9763 HIV-infected individuals from 21 cohorts shows that higher HLA-A levels confer poorer control of HIV. Elevated HLA-A expression provides enhanced levels of an HLA-A-derived signal peptide that specifically binds and determines expression levels of HLA-E, the ligand for the inhibitory NKG2A natural killer (NK) cell receptor. HLA-B haplotypes that favor NKG2A-mediated NK cell licensing (i.e., education) exacerbate the deleterious effect of high HLA-A on HIV control, consistent with NKG2A-mediated inhibition impairing NK cell clearance of HIV-infected targets. Therapeutic blockade of HLA-E: NKG2A interaction may yield benefit in HIV disease. |
领域 | 地球科学 ; 气候变化 ; 资源环境 |
收录类别 | SCI-E |
WOS记录号 | WOS:000419324700073 |
WOS关键词 | C EXPRESSION ; RECEPTOR CD94/NKG2A ; DOWN-REGULATION ; INFECTED CELLS ; NK CELLS ; TRANSPLANTATION ; ASSOCIATION ; VARIANTS ; PROTEINS ; DISEASE |
WOS类目 | Multidisciplinary Sciences |
WOS研究方向 | Science & Technology - Other Topics |
URL | 查看原文 |
引用统计 | |
文献类型 | 期刊论文 |
条目标识符 | http://119.78.100.173/C666/handle/2XK7JSWQ/197679 |
专题 | 地球科学 资源环境科学 气候变化 |
作者单位 | 1.Leidos Biomed Res Inc, Canc & Inflammat Program, Frederick Natl Lab Canc Res, Frederick, MD 21702 USA; 2.Ragon Inst Massachusetts Gen Hosp Massachusetts I, Cambridge, MA 02139 USA; 3.Univ KwaZulu Natal, Sch Lab Med & Med Sci, KwaZulu Natal Res Innovat & Sequencing Platform K, Durban, South Africa; 4.Ctr AIDS Programme Res South Africa CAPRISA, Durban, South Africa; 5.Univ Oxford, Nuffield Dept Med, Wellcome Trust Ctr Human Genet, Oxford, England; 6.Icahn Sch Med Mt Sinai, Dept Oncol Sci, Precis Immunol Inst, New York, NY 10029 USA; 7.NCI, Canc & Inflammat Program, Ctr Canc Res, NIH, Frederick, MD 21702 USA; 8.Leidos Biomed Res Inc, AIDS & Canc Virus Program, Frederick Natl Lab Canc Res, Frederick, MD 21702 USA; 9.Ecole Polytech Fed Lausanne, Sch Life Sci, Lausanne, Switzerland; 10.Swiss Inst Bioinformat, Lausanne, Switzerland; 11.Univ Calif San Francisco, Dept Med, San Francisco, CA 94143 USA; 12.Univ Calif San Francisco, Dept Epidemiol & Biostat, San Francisco, CA 94143 USA; 13.NCI, Infect & Immunoepidemiol Branch, Div Canc Epidemiol & Genet, NIH, Rockville, MD 20850 USA; 14.Northwestern Univ, Div Infect Dis, Feinberg Sch Med, Chicago, IL 60611 USA; 15.Walter Reed Army Inst Res, US Mil HIV Res Program, Silver Spring, MD 20910 USA; 16.Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD 21205 USA; 17.San Francisco Dept Publ Hlth, HIV Res Sect, San Francisco, CA 94102 USA; 18.Vanderbilt Univ, Sch Med, Nashville, TN 37232 USA; 19.African Hlth Res Inst, Durban, South Africa; 20.Univ KwaZulu Natal, HIV Pathogenesis Programme, Doris Duke Med Res Inst, Nelson R Mandela Sch Med, Durban, South Africa; 21.Max Planck Inst Infect Biol, Berlin, Germany; 22.Univ Oxford, Dept Paediat, Oxford, England; 23.Stanford Univ, Dept Struct Biol, Stanford, CA 94305 USA; 24.Stanford Univ, Dept Microbiol & Immunol, Stanford, CA 94305 USA; 25.MIT, Inst Med & Engn Sci, Cambridge, MA 02139 USA; 26.Microsoft Res, Redmond, WA 98052 USA |
推荐引用方式 GB/T 7714 | Ramsuran, Veron,39;u, Thumbi. Elevated HLA-A expression impairs HIV control through inhibition of NKG2A-expressing cells[J]. SCIENCE,2018,359(6371):86-90. |
APA | Ramsuran, Veron,&39;u, Thumbi.(2018).Elevated HLA-A expression impairs HIV control through inhibition of NKG2A-expressing cells.SCIENCE,359(6371),86-90. |
MLA | Ramsuran, Veron,et al."Elevated HLA-A expression impairs HIV control through inhibition of NKG2A-expressing cells".SCIENCE 359.6371(2018):86-90. |
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