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

Year: 2011
Type: article
Abstract: 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.
DOI: 10.1128/jvi.00412-11
Authors: Lena Fadda, Geraldine M. O'Connor, Swati Kumar, Alicja Piechocka-Trocha, Clair M. Gardiner, Mary Carrington, Daniel W. McVicar, Marcus Altfeld
Institutions: Ragon Institute of MGH, MIT and Harvard, Massachusetts General Hospital, Massachusetts Institute of Technology, National Cancer Institute, Center for Cancer Research, Trinity College Dublin, Science Applications International Corporation (United States)
Language: English
Subfield: Immunology
Open Access status: green
Funders: U.S. Department of Health and Human Services, Doris Duke Charitable Foundation, Bill and Melinda Gates Foundation, Ragon Institute of MGH, MIT and Harvard, National Institutes of Health, National Cancer Institute, National Institute of Allergy and Infectious Diseases
Awards: G3503792436, G386607036, G4117289289, NK cell mediated immune pressure in HIV-1 infection, G4585269469, G5366891077, G5888954722, Harvard University Center for AIDS Research
OpenAlex ID: W2143808879
FWCI: 4.766
Cites: 18
Cited by: 73
Related to: 10