title: Alteration of inhibitory and activating NK cell receptor expression on NK cells in HIV-infected Chinese.
abstract: Natural killer (NK) cell function, based on the expression of activating and inhibitory natural killer receptors (NKRs), may become abnormal during human immunodeficiency virus (HIV) infection. In this study, we investigated changes in receptor expression with individual and combinational analysis on NK cell subsets in HIV-infected Chinese. The results showed that natural killer group 2 member D (NKG2D) expression on total NK cells decreased significantly in HIV infection, while the expressions of natural killer group 2 member A (NKG2A) and killer cell immunoglobulin-like receptor, three domains, long cytoplasmic tail 1 (KIR3DL1) on total NK cells were not significantly different between any of the groups including HIV-positive treatment-naïve group, AIDS treatment-naïve group, HAART-treatment AIDS group and HIV-negative control group. Individual analysis of NKG2A(+) and KIR3DL1(+) cells revealed no significant differences in expression in any NK cell subsets between any of the groups, but the combinational analysis of NKG2D(-)NKG2A(+), and NKG2D(-)KIR3DL1(+) on the NK CD56(dim) cell subset in the AIDS group were increased compared to the HIV-negative control group. On the contrary, NKG2D(-)NKG2A(+) expression on the CD56(bright) subset decreased in the AIDS group compared to the control group. Highly active antiretroviral therapy (HAART) treatment almost completely restored the levels of these receptor expressions. The results indicate that the distinct alteration of activating and inhibitory NKR expression on NK cells and its subsets occurred during HIV progression. Moreover, the imbalanced change of activating and inhibitory NKRs on NK cells and its subsets may explain the impaired NK cell immunity in HIV infected individuals.
authors.affiliation: Key Laboratory of AIDS Immunology of Ministry of Health, Department of Laboratory Medicine, The First Affiliated Hospital, China Medical University, Shenyang, PR China.
authors.forename: Yongjun
authors.initials: Y
authors.lastname: Jiang
authors.forename: Lei
authors.initials: L
authors.lastname: He
authors.forename: Huan
authors.initials: H
authors.lastname: Chen
authors.forename: Tristan
authors.initials: T
authors.lastname: Bice
authors.forename: Zining
authors.initials: Z
authors.lastname: Zhang
authors.forename: Jing
authors.initials: J
authors.lastname: Liu
authors.forename: Haibo
authors.initials: H
authors.lastname: Ding
authors.forename: Xiaoxu
authors.initials: X
authors.lastname: Han
authors.forename: Hong
authors.initials: H
authors.lastname: Shang
mesh_terms: D000163:Acquired Immunodeficiency Syndrome / Q000188:drug therapy / Q000276:immunology; D000293:Adolescent; D000328:Adult; D023241:Antiretroviral Therapy, Highly Active; D044466:Asian People; D019002:CD56 Antigen / Q000378:metabolism; D016022:Case-Control Studies; D002681:China; D018450:Disease Progression; D015658:HIV Infections / Q000188:drug therapy / Q000276:immunology*; D006801:Humans; D007694:Killer Cells, Natural / Q000145:classification / Q000276:immunology*; D016131:Lymphocyte Subsets / Q000145:classification / Q000276:immunology; D008875:Middle Aged; D055654:NK Cell Lectin-Like Receptor Subfamily C / Q000378:metabolism; D055655:NK Cell Lectin-Like Receptor Subfamily K / Q000378:metabolism; D054341:Receptors, KIR3DL1 / Q000378:metabolism; D055607:Receptors, Natural Killer Cell / Q000378:metabolism*; D055815:Young Adult
chemical_list: D019002:CD56 Antigen; C515083:KIR3DL1 protein, human; C527054:KLRC1 protein, human; C527085:KLRK1 protein, human; C522918:NCAM1 protein, human; D055654:NK Cell Lectin-Like Receptor Subfamily C; D055655:NK Cell Lectin-Like Receptor Subfamily K; D054341:Receptors, KIR3DL1; D055607:Receptors, Natural Killer Cell