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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.

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  • Authors+Show Affiliations

    ,

    Key Laboratory of AIDS Immunology of Ministry of Health, Department of Laboratory Medicine, The First Affiliated Hospital, China Medical University, Shenyang, PR China.

    , , , , , , ,

    Source

    Cellular immunology 271:2 2011 pg 219-26

    MeSH

    Acquired Immunodeficiency Syndrome
    Adolescent
    Adult
    Antiretroviral Therapy, Highly Active
    Asian Continental Ancestry Group
    CD56 Antigen
    Case-Control Studies
    China
    Disease Progression
    HIV Infections
    Humans
    Killer Cells, Natural
    Lymphocyte Subsets
    Middle Aged
    NK Cell Lectin-Like Receptor Subfamily C
    NK Cell Lectin-Like Receptor Subfamily K
    Receptors, KIR3DL1
    Receptors, Natural Killer Cell
    Young Adult

    Pub Type(s)

    Journal Article
    Research Support, Non-U.S. Gov't

    Language

    eng

    PubMed ID

    21813117

    Citation

    Jiang, Yongjun, et al. "Alteration of Inhibitory and Activating NK Cell Receptor Expression On NK Cells in HIV-infected Chinese." Cellular Immunology, vol. 271, no. 2, 2011, pp. 219-26.
    Jiang Y, He L, Chen H, et al. Alteration of inhibitory and activating NK cell receptor expression on NK cells in HIV-infected Chinese. Cell Immunol. 2011;271(2):219-26.
    Jiang, Y., He, L., Chen, H., Bice, T., Zhang, Z., Liu, J., ... Shang, H. (2011). Alteration of inhibitory and activating NK cell receptor expression on NK cells in HIV-infected Chinese. Cellular Immunology, 271(2), pp. 219-26. doi:10.1016/j.cellimm.2011.06.026.
    Jiang Y, et al. Alteration of Inhibitory and Activating NK Cell Receptor Expression On NK Cells in HIV-infected Chinese. Cell Immunol. 2011;271(2):219-26. PubMed PMID: 21813117.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Alteration of inhibitory and activating NK cell receptor expression on NK cells in HIV-infected Chinese. AU - Jiang,Yongjun, AU - He,Lei, AU - Chen,Huan, AU - Bice,Tristan, AU - Zhang,Zining, AU - Liu,Jing, AU - Ding,Haibo, AU - Han,Xiaoxu, AU - Shang,Hong, Y1 - 2011/07/20/ PY - 2010/11/11/received PY - 2011/06/28/revised PY - 2011/06/29/accepted PY - 2011/8/5/entrez PY - 2011/8/5/pubmed PY - 2011/12/13/medline SP - 219 EP - 26 JF - Cellular immunology JO - Cell. Immunol. VL - 271 IS - 2 N2 - 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. SN - 1090-2163 UR - https://www.unboundmedicine.com/medline/citation/21813117/Alteration_of_inhibitory_and_activating_NK_cell_receptor_expression_on_NK_cells_in_HIV_infected_Chinese_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0008-8749(11)00177-8 DB - PRIME DP - Unbound Medicine ER -