title: Expansion of CD1d-restricted NKT cells in patients with primary HIV-1 infection treated with interleukin-2.
abstract: Innate CD1d-restricted natural killer T (NKT) cells are infected and lost in HIV-1-infected patients, and this could contribute to HIV-1 pathogenesis because NKT cells play an important role in directing both adaptive and innate immunity. Administration of interleukin-2 (IL-2) to HIV-1-infected patients leads to substantial and sustained CD4+ T-cell expansion, involving both naive and memory cells. We investigated whether IL-2 treatment could restore the NKT cell compartment in patients with primary HIV-1 infection. We show that IL-2 combined with effective antiretroviral therapy (ART) resulted in significant expansion of CD1d-restricted NKT cells. Expansion occurred in both the CD4- and CD4+ subsets of NKT cells, and expanded cells expressed the CD161 maturation marker while expression of the HIV coreceptor CCR5 was reduced. These data indicate that IL-2 treatment in combination with effective ART is beneficial for the restoration of innate NKT cell immunity in patients with primary HIV-1 infection.
authors.affiliation: CIM, Department of Medicine, F59, Karolinska Institute, Karolinska University Hospital, Huddinge, 14186 Stockholm, Sweden. markus.moll@ki.se
authors.forename: Markus
authors.initials: M
authors.lastname: Moll
authors.forename: Jennifer
authors.initials: J
authors.lastname: Snyder-Cappione
authors.forename: Gerald
authors.initials: G
authors.lastname: Spotts
authors.forename: Frederick M
authors.initials: FM
authors.lastname: Hecht
authors.forename: Johan K
authors.initials: JK
authors.lastname: Sandberg
authors.forename: Douglas F
authors.initials: DF
authors.lastname: Nixon
mesh_terms: D000328:Adult; D019380:Anti-HIV Agents / Q000008:administration & dosage* / Q000276:immunology; D018949:Antigens, CD1 / Q000276:immunology; D055610:Antigens, CD1d; D000954:Antigens, Surface / Q000276:immunology; D000970:Antineoplastic Agents / Q000008:administration & dosage*; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology* / Q000821:virology; D004359:Drug Therapy, Combination; D005260:Female; D005786:Gene Expression Regulation / Q000187:drug effects / Q000276:immunology; D015658:HIV Infections / Q000188:drug therapy* / Q000276:immunology; D015497:HIV-1 / Q000276:immunology; D006801:Humans; D007111:Immunity, Cellular / Q000187:drug effects / Q000276:immunology; D007113:Immunity, Innate / Q000187:drug effects / Q000276:immunology; D007156:Immunologic Memory / Q000187:drug effects / Q000276:immunology; D007376:Interleukin-2 / Q000008:administration & dosage* / Q000276:immunology; D007694:Killer Cells, Natural / Q000276:immunology* / Q000821:virology; D037181:Lectins, C-Type / Q000276:immunology; D008297:Male; D008875:Middle Aged; D055651:NK Cell Lectin-Like Receptor Subfamily B; D019713:Receptors, CCR5 / Q000276:immunology; D020127:Recovery of Function / Q000187:drug effects / Q000276:immunology
chemical_list: D019380:Anti-HIV Agents; D018949:Antigens, CD1; D055610:Antigens, CD1d; D000954:Antigens, Surface; D000970:Antineoplastic Agents; C526877:CD1D protein, human; D007376:Interleukin-2; C527203:KLRB1 protein, human; D037181:Lectins, C-Type; D055651:NK Cell Lectin-Like Receptor Subfamily B; D019713:Receptors, CCR5