کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
5533133 1402102 2017 8 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Aberrant NKG2D expression with IL-17 production of CD4+ T subsets in patients with type 2 diabetes
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی بیولوژی سلول
پیش نمایش صفحه اول مقاله
Aberrant NKG2D expression with IL-17 production of CD4+ T subsets in patients with type 2 diabetes
چکیده انگلیسی

Type 2 diabetes (T2D) is a systemic inflammatory disease. Although the natural killer group 2, member D (NKG2D) receptor, was not expressed normally on CD4+ T cells, the aberrant expression was found in pathological conditions such as in auto-immune diseases. However, the involvement of NKG2D in pathogenesis of T2D is unclear. We hypothesize that there is an inflammatory CD4+ T cell subpopulation expressing NKG2D and producing interleukin (IL)-17 in T2D. NKG2D expression on CD4+ T cells and their subsets were analyzed by multi-color staining using flow cytometry. Lymphocytes were activated by phorbol-12-myristate-13-acetate (PMA) and ionomycin, and were stained for intracellular IL-17. To investigate the mechanism of IL-17 production, patients' lymphocytes were stimulated using specific anti-T cell receptor (TCR) alone, anti-NKG2D alone or a combination of the two antibodies. CD4+ T cells and particularly, CD4 + CD28null T subset of T2D patients were highly expressed NKG2D and more prevalent compared to non-diabetic individuals (ND) (P = 0.039 and P = 0.022, respectively). Significantly higher percentages of CD4 + CD28nullNKG2D + T cells of patients produced IL-17 when compared to those of ND (P = 0.024) and were positively correlated with the level of glycated hemoglobin A1c (HbA1c) (R2 = 0.386, P = 0.041). Additionally, this cell population could be stimulated by specific monoclonal anti-NKG2D to produce IL-17. In conclusion, CD4 + CD28nullNKG2D+ T cells were expanded in T2D, especially in patients with poor glycemic control. NKG2D may be one of the surrogate co-stimulatory receptors leading to irregular inflammatory function producing IL-17. An IL-17 producing CD4 + CD28nullNKG2D + T cells may potentially be involved in pathogenesis and drive severity of the disease with the glycemic dependence. This particular cell type could be targeted for prognostic or therapeutic purposes.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Immunobiology - Volume 222, Issue 10, October 2017, Pages 944-951
نویسندگان
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