title: Alteration of inhibitory and activating natural killer cell receptor expression on T cells in human immunodeficiency virus-infected Chinese.
abstract: T cell expression of NKRs can trigger or inhibit cell-mediated cytotoxicity. However, few studies on T lymphocyte NKR expression in HIV infection exist. Here, we examined the expression patterns of NKG2D, NKG2A, and KIR3DL1 on CD8⁺ and CD3⁺CD8⁻ cells by multicolor flow cytometry in groups of patients with HIV, AIDS or HAART-treated AIDS, as well as HIV-negative normal controls. Individual analysis of KIR3DL1 on CD3⁺ CD8⁺ or CD3⁺CD8⁻ cells revealed no significant differences among any of the groups (P > 0.05). In contrast, the percentage of NKG2A⁺NKG2D⁻CD8⁺ T cells was higher in the AIDS group than in the HIV-negative normal control group (P < 0.01). Meanwhile, the prevalence of NKG2D⁺ NKG2A⁻ CD8⁺ T cells was lower in the AIDS group than in HIV-negative normal controls (P < 0.001). Similar results were also observed for the percentage of NKG2A⁺ NKG2D⁻ on CD3⁺ CD8⁻ cells. However, in contrast to CD8⁺ T cells, the frequencies of NKG2D⁺ NKG2A⁻ on CD3⁺CD8⁻ cells were higher in AIDS and HIV patients than in HIV-negative normal controls (P < 0.01, P < 0.05, respectively). The percentage of NKG2A⁺NKG2⁻CD8⁺ T cells was negatively correlated with CD4⁺T cell counts (r=-0.499, P < 0.01), while the percentage of NKG2D⁺NKG2A⁻CD8⁺ T cells was positively correlated with CD4⁺ T cell counts (r= 0.494, P < 0.01). The percentage of NKG2D⁺NKG2A⁻CD3⁺CD8⁻ T cells was also positively correlated with viral load (r= 0.527, P < 0.01) and negatively correlated with CD4⁺ T cell counts (r=-0.397, P < 0.05). Finally, HAART treatment reversed the changes in NKR expression caused by HIV infection. These results indicate that the expression of NKRs on T cells may be correlated with HIV disease progression.
authors.affiliation: Key Laboratory of AIDS Immunology of Ministry of Health, Department of Laboratory Medicine, The First Hospital of China Medical University, Shenyang, China.
authors.forename: Yongjun
authors.initials: Y
authors.lastname: Jiang
authors.forename: Shanshan
authors.initials: S
authors.lastname: Wu
authors.forename: Fangyuan
authors.initials: F
authors.lastname: Zhou
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: D019380:Anti-HIV Agents / Q000627:therapeutic use; D023241:Antiretroviral Therapy, Highly Active; D002681:China; D015870:Gene Expression / Q000187:drug effects*; D006678:HIV / Q000235:genetics / Q000276:immunology / Q000502:physiology*; D015658:HIV Infections / Q000188:drug therapy / Q000235:genetics / Q000276:immunology* / Q000821:virology; D006801:Humans; D055607:Receptors, Natural Killer Cell / Q000235:genetics* / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology* / Q000821:virology
chemical_list: D019380:Anti-HIV Agents; D055607:Receptors, Natural Killer Cell