title: Modulation of expression of the MHC class I-binding natural killer cell receptors, and NK activity in relation to viral load in HIV-infected/AIDS patients.
abstract: The natural killer (NK) cells play an important role in viral infections via their spontaneous cytolytic activity against virus-infected cells as well as via secreting a variety of soluble mediators. The MHC class I-binding NK receptors of these cells have emerged as the most important regulators of the effector activities of cytolytic cells (both NK and CTL). We have studied the modulation of NK activity and the expression of NK receptors in HIV-infected/AIDS patients and report here that the NK activities of the patients with the lowest plasma HIV load were minimal and vice versa, suggesting a decrease in this activity following suppression of HIV replication. Interestingly, the NK activity correlated negatively with the peripheral blood CD4+ T-cell counts of these patients. Furthermore, these patients showed decreased percentages of CD56+ cells expressing NK receptors of the immunoglobulin superfamily, whereas the percentages of CD8+ cells expressing these receptors were increased. Moreover, the expression of C-type lectin-like NK receptor-associated invariant molecule CD94 was increased on CD8+ cells in these patients as compared with HIV-seronegative controls. These changes in the expression of NK receptors were also evident within groups of these patients having different viral loads. These results show, for the first time, decreased innate immunity and changes in the expression of NK receptors on cytolytic cells in relation to viral burden in HIV-infected/AIDS patient.
authors.affiliation: Laboratory of Immunovirology, Pediatric Research Center, Ste-Justine Hospital, Montreal, QC, H3T 1C5 Canada.
authors.forename: R
authors.initials: R
authors.lastname: Ahmad
authors.forename: S T
authors.initials: ST
authors.lastname: Sindhu
authors.forename: P
authors.initials: P
authors.lastname: Tran
authors.forename: E
authors.initials: E
authors.lastname: Toma
authors.forename: R
authors.initials: R
authors.lastname: Morisset
authors.forename: J
authors.initials: J
authors.lastname: Menezes
authors.forename: A
authors.initials: A
authors.lastname: Ahmad
mesh_terms: D000328:Adult; D015703:Antigens, CD / Q000378:metabolism; D019002:CD56 Antigen / Q000378:metabolism; D018414:CD8-Positive T-Lymphocytes / Q000378:metabolism; D015658:HIV Infections / Q000276:immunology* / Q000821:virology; D015497:HIV-1 / Q000276:immunology / Q000502:physiology*; D015395:Histocompatibility Antigens Class I / Q000378:metabolism*; D006801:Humans; D007694:Killer Cells, Natural / Q000276:immunology* / Q000378:metabolism; D037181:Lectins, C-Type; D008562:Membrane Glycoproteins / Q000378:metabolism; D051920:NK Cell Lectin-Like Receptor Subfamily D; D009336:Necrosis; D011971:Receptors, Immunologic / Q000378:metabolism*; D019562:Viral Load
chemical_list: D015703:Antigens, CD; D019002:CD56 Antigen; D015395:Histocompatibility Antigens Class I; C497869:KLRD1 protein, human; D037181:Lectins, C-Type; D008562:Membrane Glycoproteins; D051920:NK Cell Lectin-Like Receptor Subfamily D; D011971:Receptors, Immunologic