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Extra info for Nature Reviews Immunology 11, 155 (March 2011)
Sample text
J. Exp. Med. 204, 3027–3036 (2007). 86. Long, B. R. et al. Conferral of enhanced natural killer cell function by KIR3DS1 in early human immunodeficiency virus type 1 infection. J. Virol. 82, 4785–4792 (2008). 87. Boulet, S. et al. Increased proportion of KIR3DS1 homozygotes in HIV‑exposed uninfected individuals. AIDS 22, 595–599 (2008). 88. Gillespie, G. M. et al. Lack of KIR3DS1 binding to MHC class I Bw4 tetramers in complex with CD8+ T cell epitopes. AIDS Res. Hum. Retroviruses 23, 451–455 (2007).
However, this discrepancy could be explained by the interactions of KIRs with HLA molecules during NK cell development. As described in bOX 1, developing NK cells undergo a licensing proc‑ ess, in which engagement of inhibitory KIRs by HLA molecules arms NK cells with functional capacity 97–99. The strength of interaction between inhibitory KIRs and HLA molecules at this licensing step proportion‑ ately enhances later functional capacity. Indeed, studies have shown that KIR3DL1+ NK cells from individuals homozygous for HLA‑Bw4 respond more potently to mHC class I‑negative cells than NK cells from individu‑ als expressing only one copy or no copies of HLA‑Bw4 (Ref.
74. Kottilil, S. et al. Innate immunity in human immunodeficiency virus infection: effect of viremia on natural killer cell function. J. Infect. Dis. 187, 1038–1045 (2003). 75. Portales, P. et al. Interferon‑α restores HIV‑induced alteration of natural killer cell perforin expression in vivo. AIDS 17, 495–504 (2003). 76. De Maria, A. et al. The impaired NK cell cytolytic function in viremic HIV‑1 infection is associated with a reduced surface expression of natural cytotoxicity receptors (NKp46, NKp30 and NKp44).