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Increased Th22 cells are independently associated with Thl7 cells in type 1 diabetes

机译:在1型糖尿病中,增加的Th22细胞与Thl7细胞独立相关

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摘要

Type 1 diabetes (T1D) is perceived as an autoimmune disease caused by T cell-mediated destruction of the insulin-producing pancreatic beta cells. However, the number of inflammatory T cells in blood, as well as the relative importance of each cell type is unclear. Forty-two patients with T1D and 30 controls were enrolled. Circulating primary CD4~+ or CD8~+ T cells were quantified with 5-color flow cytometry. Serum IL-22 and IL-17 levels were examined by ELISA. Serum autoantibodies were measured by radio-binding assays, using ~(35)S-labeled glutamic acid decarboxylase-65 (GAD65), protein tyrosine phosphatase-2 (IA-2), and zinc transporter 8 (ZnT8). Thl7-Th22 and Tcl-Tcl7 were significantly elevated in patients with T1D compared to control subjects, while there were no significant differences in Thl cells. The levels of these T cells in different stages of T1D were investigated. Th22 cells showed a positive correlation with Thl7 cells in T1D patients. However, we did not find any correlation between IL-17 and IL-22 in sera. Autoantibodies were not significantly different between patients with early T1D and those who have had it for a longer duration. This study indicates that Th22 may contribute to the pathogenesis of T1D. Blockade of Th22 cells might be of clinical profit in T1D patients.
机译:1型糖尿病(T1D)被认为是由T细胞介导的产生胰岛素的胰岛β细胞破坏引起的自身免疫性疾病。但是,尚不清楚血液中炎性T细胞的数量以及每种细胞类型的相对重要性。纳入了42例T1D患者和30例对照。用五色流式细胞仪定量循环的原代CD4 +或CD8 + T细胞。通过ELISA检查血清IL-22和IL-17水平。使用〜(35)S标记的谷氨酸脱羧酶65(GAD65),蛋白酪氨酸磷酸酶2(IA-2)和锌转运蛋白8(ZnT8)通过放射结合测定法测量血清自身抗体。与对照组相比,T1D患者的Thl7-Th22和Tcl-Tcl7显着升高,而Th1细胞没有显着差异。研究了这些T细胞在T1D不同阶段的水平。在T1D患者中,Th22细胞与Thl7细胞呈正相关。但是,我们在血清中未发现IL-17和IL-22之间的任何相关性。早期T1D患者与持续时间较长的患者之间的自身抗体无显着差异。这项研究表明Th22可能与T1D的发病机制有关。阻断Th22细胞可能在T1D患者中具有临床价值。

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