title: High frequency of activated natural killer and natural killer T-cells in patients with new onset of type 2 diabetes mellitus.
abstract: Chronic low-grade inflammation is crucial for the development of insulin resistance and type 2 diabetes mellitus (T2DM), and immunocompetent cells, such as T-cells, B-cells, mast cells and macrophages, regulate the pathogenesis of T2DM. However, little is known about the role of natural killer (NK) and natural killer T (NKT) cells in the pathogenic process of T2DM. A total of 16 patients with new onset T2DM and nine healthy subjects were recruited, and the frequency of peripheral blood activated and inhibitory NK and NKT cells in individual subjects was determined by flow cytometry. The frequency of spontaneous and inducible interferon gamma (IFN-γ) and CD107a(+) NK cells was further examined, and the potential association of the frequency of NK cells with clinical measures was analyzed. While there was no significant difference in the frequency of peripheral blood NK and NKT cells between patients and controls, the frequency of NKG2D(+) NK and NKT cells in patients was significantly higher than those in the controls (P = 0.011). In contrast, the frequency of NKG2A(+) and KIR2DL3(+) inhibitory NK and NKT cells in patients was significantly lower than those in the controls (P = 0.002, P < 0.0001, respectively). Furthermore, the frequencies of NKG2D(+) NK cells were correlated significantly with the values of body mass index in patients. Moreover, the frequencies of spontaneous and inducible CD107a(+), but not IFN-γ-secreting, NK cells in patients were significantly higher than those in the controls (P < 0.004, P < 0.0001). Our data indicated that a higher frequency of activated NK cells may participate in the obesity-related chronic inflammation involved in the pathogenesis of T2DM.
authors.affiliation: The Second Part of First Hospital, Jilin University, Changchun 130031,  China.
authors.forename: Hui
authors.initials: H
authors.lastname: Guo
authors.forename: Bingchuan
authors.initials: B
authors.lastname: Xu
authors.forename: Lichao
authors.initials: L
authors.lastname: Gao
authors.forename: Xiguang
authors.initials: X
authors.lastname: Sun
authors.forename: Xiaozhang
authors.initials: X
authors.lastname: Qu
authors.forename: Xiaowei
authors.initials: X
authors.lastname: Li
authors.forename: Shumei
authors.initials: S
authors.lastname: Liu
authors.forename: Junyan
authors.initials: J
authors.lastname: Feng
authors.forename: Juan
authors.initials: J
authors.lastname: Wang
authors.forename: Ying
authors.initials: Y
authors.lastname: Tang
authors.forename: Guoqiang
authors.initials: G
authors.lastname: Yan
authors.forename: Xiuzhu
authors.initials: X
authors.lastname: Gao
authors.forename: Yanfang
authors.initials: Y
authors.lastname: Jiang
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D015992:Body Mass Index; D015550:Cell Degranulation; D003602:Cytotoxicity, Immunologic; D003924:Diabetes Mellitus, Type 2 / Q000276:immunology*; D005260:Female; D006801:Humans; D007371:Interferon-gamma / Q000378:metabolism; D007694:Killer Cells, Natural / Q000276:immunology* / Q000378:metabolism; D008213:Lymphocyte Activation; D052118:Lysosomal-Associated Membrane Protein 1 / Q000097:blood; D008297:Male; D008875:Middle Aged; D055654:NK Cell Lectin-Like Receptor Subfamily C / Q000097:blood; D055655:NK Cell Lectin-Like Receptor Subfamily K / Q000097:blood; D055611:Natural Killer T-Cells / Q000276:immunology* / Q000378:metabolism; D054344:Receptors, KIR2DL3 / Q000097:blood; D055815:Young Adult
chemical_list: C515078:KIR2DL3 protein, human; C527085:KLRK1 protein, human; D052118:Lysosomal-Associated Membrane Protein 1; D055654:NK Cell Lectin-Like Receptor Subfamily C; D055655:NK Cell Lectin-Like Receptor Subfamily K; D054344:Receptors, KIR2DL3; D007371:Interferon-gamma