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Letter

Nature Genetics 31, 429–434 (1 August 2002) | doi:10.1038/ng934

Epistatic interaction between KIR3DS1 and HLA-B delays the progression to AIDS

Maureen P. Martin , Xiaojiang Gao , Jeong-Hee Lee , George W. Nelson , Roger Detels , James J. Goedert , Susan Buchbinder , Keith Hoots , David Vlahov , John Trowsdale , Michael Wilson , Stephen J. O'Brien & Mary Carrington

Natural killer (NK) cells provide defense in the early stages of the innate immune response against viral infections by producing cytokines and causing cytotoxicity. The killer immunoglobulin-like receptors (KIRs) on NK cells regulate the inhibition and activation of NK-cell responses through recognition of human leukocyte antigen (HLA) class I molecules on target cells KIR and HLA loci are both highly polymorphic, and some HLA class I products bind and trigger cell-surface receptors specified by KIR genes.