Biron, C.A., Nguyen, K.B., Pien, G.C., Cousens, L.P. & Salazar-Mather, T.P. Natural killer cells in antiviral defense: function and regulation by innate cytokines. Annu. Rev. Immunol. 17, 189–220 (1999).
Lanier, L.L. NK cell recognition. Annu. Rev. Immunol. 23, 225–274 (2005).
Colucci, F., Di Santo, J.P. & Leibson, P.J. Natural killer cell activation in mice and men: different triggers for similar weapons? Nat. Immunol. 3, 807–813 (2002).
Vilches, C. & Parham, P. KIR: diverse, rapidly evolving receptors of innate and adaptive immunity. Annu. Rev. Immunol. 20, 217–251 (2002).
Gumperz, J.E. et al. Conserved and variable residues within the Bw4 motif of HLA-B make separable contributions to recognition by the NKB1 killer cell-inhibitory receptor. J. Immunol. 158, 5237–5241 (1997).
Carr, W.H., Pando, M.J. & Parham, P. KIR3DL1 polymorphisms that affect NK cell inhibition by HLA-Bw4 ligand. J. Immunol. 175, 5222–5229 (2005).
Cella, M., Longo, A., Ferrara, G.B., Strominger, J.L. & Colonna, M. NK3-specific natural killer cells are selectively inhibited by Bw4- positive HLA alleles with isoleucine 80. J. Exp. Med. 180, 1235–1242 (1994).
Valiante, N.M. et al. Functionally and structurally distinct NK cell receptor repertoires in the peripheral blood of two human donors. Immunity 7, 739–751 (1997).
Gardiner, C.M. et al. Different NK cell surface phenotypes defined by the DX9 antibody are due to KIR3DL1 gene polymorphism. J. Immunol. 166, 2992–3001 (2001).
Yawata, M. et al. Roles for HLA and KIR polymorphisms in natural killer cell repertoire selection and modulation of effector function. J. Exp. Med. 203, 633–645 (2006).
Pando, M.J., Gardiner, C.M., Gleimer, M., McQueen, K.L. & Parham, P. The protein made from a common allele of KIR3DL1 (3DL1*004) is poorly expressed at cell surfaces due to substitution at positions 86 in Ig domain 0 and 182 in Ig domain 1. J. Immunol. 171, 6640–6649 (2003).
Carrington, M. & O'Brien, S.J. The influence of HLA genotype on AIDS. Annu. Rev. Med. 54, 535–551 (2003).
Goulder, P.J. & Watkins, D.I. HIV and SIV CTL escape: Implications for vaccine design. Nat. Rev. Immunol. 4, 630–640 (2004).
Flores-Villanueva, P.O. et al. Control of HIV-1 viremia and protection from AIDS are associated with HLA-Bw4 homozygosity. Proc. Natl. Acad. Sci. USA 98, 5140–5145 (2001).
Rammensee, H., Bachmann, J., Emmerich, N.P., Bachor, O.A. & Stevanovic, S. SYFPEITHI: database for MHC ligands and peptide motifs. Immunogenetics 50, 213–219 (1999).
O'Brien, S.J., Gao, X. & Carrington, M. HLA and AIDS: a cautionary tale. Trends Mol. Med. 7, 379–381 (2001).
Martin, M.P. et al. Epistatic interaction between KIR3DS1 and HLA-B delays the progression to AIDS. Nat. Genet. 31, 429–434 (2002).
Qi, Y. et al. KIR/HLA pleiotropism: Protection against both HIV and opportunistic infections. PLoS Pathog. 2, e79 (2006).
Anfossi, N. et al. Human NK cell education by inhibitory receptors for MHC class I. Immunity 25, 331–342 (2006).
Fernandez, N.C. et al. A subset of natural killer cells achieves self-tolerance without expressing inhibitory receptors specific for self-MHC molecules. Blood 105, 4416–4423 (2005).
Kim, S. et al. Licensing of natural killer cells by host major histocompatibility complex class I molecules. Nature 436, 709–713 (2005).
Storey, J.D. & Tibshirani, R. Statistical significance for genomewide studies. Proc. Natl. Acad. Sci. USA 100, 9440–9445 (2003).
Gao, X. et al. AIDS restriction HLA allotypes target distinct intervals of HIV-1 pathogenesis. Nat. Med. 11, 1290–1292 (2005).
Gao, X. et al. Effect of a single amino acid change in MHC class I molecules on the rate of progression to AIDS. N. Engl. J. Med. 344, 1668–1675 (2001).
Lopez-Vazquez, A. et al. Interaction between KIR3DL1 and HLA-B*57 supertype alleles influences the progression of HIV-1 infection in a Zambian population. Hum. Immunol. 66, 285–289 (2005).
Jennes, W. et al. Cutting edge: resistance to HIV-1 infection among African female sex workers is associated with inhibitory KIR in the absence of their HLA ligands. J. Immunol. 177, 6588–6592 (2006).
Dorfman, J.R. & Raulet, D.H. Acquisition of Ly49 receptor expression by developing natural killer cells. J. Exp. Med. 187, 609–618 (1998).
Held, W., Dorfman, J.R., Wu, M.F. & Raulet, D.H. Major histocompatibility complex class I-dependent skewing of the natural killer cell Ly49 receptor repertoire. Eur. J. Immunol. 26, 2286–2292 (1996).
Parham, P. Taking license with natural killer cell maturation and repertoire development. Immunol. Rev. 214, 155–160 (2006).
Raulet, D.H. & Vance, R.E. Self-tolerance of natural killer cells. Nat. Rev. Immunol. 6, 520–531 (2006).
Yokoyama, W.M. & Kim, S. How do natural killer cells find self to achieve tolerance? Immunity 24, 249–257 (2006).
Khakoo, S.I. et al. HLA and NK cell inhibitory receptor genes in resolving hepatitis C virus infection. Science 305, 872–874 (2004).
Carrington, M. et al. Hierarchy of resistance to cervical neoplasia mediated by combinations of killer immunoglobulin-like receptor and human leukocyte antigen loci. J. Exp. Med. 201, 1069–1075 (2005).
Klein, J., Satta, Y., O'hUigin, C. & Takahata, N. The molecular descent of the major histocompatibility complex. Annu. Rev. Immunol. 11, 269–295 (1993).
Kiepiela, P. et al. Dominant influence of HLA-B in mediating the potential co-evolution of HIV and HLA. Nature 432, 769–775 (2004).
Yawata, M., Yawata, N., Abi-Rached, L. & Parham, P. Variation within the human killer cell immunoglobulin-like receptor (KIR) gene family. Crit. Rev. Immunol. 22, 463–482 (2002).
Abi-Rached, L. & Parham, P. Natural selection drives recurrent formation of activating killer cell immunoglobulin-like receptor and Ly49 from inhibitory homologues. J. Exp. Med. 201, 1319–1332 (2005).
Khakoo, S.I. et al. Rapid evolution of NK cell receptor systems demonstrated by comparison of chimpanzees and humans. Immunity 12, 687–698 (2000).
Phair, J. et al. Acquired immune deficiency syndrome occurring within 5 years of infection with human immunodeficiency virus type-1: the Multicenter AIDS Cohort Study. J. Acquir. Immune Defic. Syndr. 5, 490–496 (1992).
Goedert, J.J. et al. A prospective study of human immunodeficiency virus type 1 infection and the development of AIDS in subjects with hemophilia. N. Engl. J. Med. 321, 1141–1148 (1989).
Buchbinder, S.P., Katz, M.H., Hessol, N.A., O'Malley, P.M. & Holmberg, S.D. Long-term HIV-1 infection without immunologic progression. AIDS 8, 1123–1128 (1994).
Vlahov, D. et al. Prognostic indicators for AIDS and infectious disease death in HIV-infected injection drug users: plasma viral load and CD4+ cell count. J. Am. Med. Assoc. 279, 35–40 (1998).
Emu, B. et al. Phenotypic, functional, and kinetic parameters associated with apparent T-cell control of human immunodeficiency virus replication in individuals with and without antiretroviral treatment. J. Virol. 79, 14169–14178 (2005).
Migueles, S.A. et al. HIV-specific CD8+ T cell proliferation is coupled to perforin expression and is maintained in nonprogressors. Nat. Immunol. 3, 1061–1068 (2002).
Council of State and Territorial Epidemiologists; AIDS Program, Center for Infectious Diseases. Revision of the CDC surveillance case definition for acquired immunodeficiency syndrome. MMWR Morb. Mortal. Wkly. Rep. 36(suppl. 1), 1S–15S (1987).