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CUTTING EDGE |
* Medical Research Council Human Immunology Unit, Weatherall Institute of Molecular Medicine, Oxford, United Kingdom;
Laboratory of Genomic Diversity, Science Applications International Corporation-Frederick, National Cancer Institute, Frederick, MD 21702;
Johns Hopkins University School of Medicine, Baltimore, MD 21205;
Department of Structural Biology and Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305;
¶ Department of HIV/Genitourinary Medicine, The Guy’s, Kings’, and St. Thomas’ School of Medicine, London, United Kingdom;
|| Laboratory of Experimental Immunology, National Cancer Institute, Frederick, MD 21702; and
# Division of Structural Biology, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan
Although it is clear that KIR3DL1 recognizes Bw4+ HLA-B, the role of Bw4+ HLA-A allotypes as KIR3DL1 ligands is controversial. We therefore examined the binding of tetrameric HLA-A and –B complexes, including HLA*2402, a common Bw4+ HLA-A allotype, to KIR3DL1*001, *005, *007, and *1502 allotypes. Only Bw4+ tetramers bound KIR3DL1. Three of four HLA-A*2402 tetramers bound one or more KIR3DL1 allotypes and all four KIR3DL1 allotypes bound to one or more HLA-A*2402 tetramers, but with different binding specificities. Only KIR3DL1*005 bound both HLA-A*2402 and HLA-B*5703 tetramers. HLA-A*2402-expressing target cells were resistant to lysis by NK cells expressing KIR3DL1*001 or *005. This study shows that HLA-A*2402 is a ligand for KIR3DL1 and demonstrates how the binding of KIR3DL1 to Bw4+ ligands depends upon the bound peptide as well as HLA and KIR3DL1 polymorphism.
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1 This work was funded by the Medical Research Council, United Kingdom and in part with federal funds under the Intramural Research Program of the National Cancer Institute, National Institutes of Health under Contract N01-CO-12400. H.T. was funded by the Royal Thai Government.
2 The content of this publication does not necessarily reflect the views or policies of the Department of Health and Human Services, nor does mention of trade names, commercial products, or organizations imply endorsements by the U.S. government.
3 T.D. and S.R.-J. contributed equally to this work.
4 Address correspondence and reprint requests to Dr. Tao Dong and Dr. Sarah Rowland-Jones, Medical Research Council Human Immunology Unit, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, Oxford OX3 9DS, United Kingdom. E-mail addresses: TDong{at}hammer.imm.ox.ac.uk and sarah.rowland-jones{at}ndm.ox.ac.uk
5 Abbreviations used in this paper: KIR, killer Ig-like receptor; LTNP, long-term nonprogressor; rh, recombinant human.
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