Differential regulation of killer cell Ig-like receptors and CD94 lectin-like dimers on NK and T lymphocytes from HIV-1-infected individuals

NK and T lymphocytes share various cell surface receptors, including NK rec eptors for MHC class I molecules (NKR). NKR include killer cell Ig-like rec eptors (KIR) and lectin-like dimers which are composed of the invariant CD9 4 associated with a variety of NKG2 molecules. The combination of KIR and C D94/NKG2 dimers expressed on NK and T cell subsets defines a repertoire of MHC class I recognition. Engagement of NKR by cognate MHC class I molecules governs T and NK cell activation. We investigated the NKR distribution on NK and T cell subsets from uninfected and HIV-infected individuals, accordi ng to the clinical status, the absolute numbers of CD4(+) T cells as well a s the plasmatic viral load of the patients. We show that the KIR distributi on on NK cells is not affected by HIV-1 infection, whereas the absolute num bers of T cells expressing specific KIR members (CD158b, p70) transiently i ncrease in early stages of HIV infection. By contrast, the percentages of N K and T cells which express CD94 dimers increase in parallel with the disea se. These results document a differential regulation of KIR and CD94 lectin -like dimers during the course of a chronic viral infection in humans and f urther suggest that both types of NKR are independently regulated.