Common HIV-1 Peptide Variants Mediate Differential Binding of KIR3DL1 to HLA-Bw4 Molecules

被引：56

作者：

Fadda, Lena ^{[1
]}

O'Connor, Geraldine M. ^{[2
]}

Kumar, Swati ^{[1
]}

Piechocka-Trocha, Alicja ^{[1
]}

Gardiner, Clair M. ^{[3
]}

Carrington, Mary ^{[1
,4
]}

McVicar, Daniel W. ^{[2
]}

Altfeld, Marcus ^{[1
]}

机构：

[1] Massachusetts Gen Hosp, Ragon Inst MGH MIT & Harvard, Charlestown, MA 02129 USA

[2] NCI, Canc & Inflammat Program, Ctr Canc Res, Frederick, MD 21702 USA

[3] Trinity Coll Dublin, Sch Biochem & Immunol, Dublin, Ireland

[4] NCI, Canc & Inflammat Program, Expt Immunol Lab, SAIC Frederick Inc, Frederick, MD 21701 USA

来源：

JOURNAL OF VIROLOGY | 2011年 / 85卷 / 12期

基金：

美国国家卫生研究院;

关键词：

HLA-B; NK CELLS; INFECTION; MUTATION; RECEPTOR; AIDS; SUBTYPES; ESCAPE; GAG;

D O I：

10.1128/JVI.00412-11

中图分类号：

Q93 [微生物学];

学科分类号：

071005 ; 100705 ;

摘要：

Epidemiological studies have shown the protective effect of KIR3DL1/HLA-Bw4 genotypes in human immunodeficiency virus type 1 (HIV-1) infection; however, the functional correlates for the protective effect remain unknown. We investigated whether human leukocyte antigen (HLA)-Bw4-presented HIV-1 peptides could affect the interaction between the inhibitory natural killer (NK) cell receptor KIR3DL1 and its ligand HLA-Bw4. Distinct HIV-1 epitopes differentially modulated the binding of KIR3DL1 to HLA-Bw4. Furthermore, cytotoxic T lymphocyte (CTL) escape mutations within the immunodominant HLA-B57 (Bw4)-restricted Gag epitope TSTLQEQIGW abrogated KIR3DL1 binding to HLA-B57, suggesting that sensing of CTL escape variants by NK cells can contribute to the protective effect of the KIR3DL1/HLA-Bw4 compound genotype.

引用

页码：5970 / 5974

页数：5

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