Abstract：
UNASSIGNED: CD83 are closely related to the pathogenesis of immune thrombocytopenia (ITP), but the exact mechanism remains unclear.
UNASSIGNED: To explore the relationship between CD83 and CD4+ T cell subsets and clarify the role of CD83 in the pathogenesis of ITP.
UNASSIGNED: RT-qPCR and Flow cytometry were used to illustrate CD83 expression. The downregulation and overexpression of DC-CD83 were co-cultured with CD4+ T cells to detect cell proliferation, co-cultured supernatant cytokines and Tregs expression.
UNASSIGNED: The results indicate that the ITP patients showed higher expression of CD83 than the healthy controls. The proliferation of CD4+ T cells was inhibited by downregulation of DCs-CD83 but promoted by overexpression of DCs-CD83. siRNA-CD83 inhibited proinflammatory IFN-γ and IL-17 secretion while raising TGF-β, IL-10 concentrations. Overexpression of DCs-CD83 promoted Tregs expression.
UNASSIGNED: The Th1/Th2 and Th17/Tregs polarization were reversed via interfering DCs with siRNA-CD83. CD83 plays an important role in ITP pathogenesis, suggesting novel treatment for ITP patients.
UNASSIGNED: To explore the relationship between CD83 and CD4+ T cell subsets and clarify the role of CD83 in the pathogenesis of ITP.
UNASSIGNED: RT-qPCR and Flow cytometry were used to illustrate CD83 expression. The downregulation and overexpression of DC-CD83 were co-cultured with CD4+ T cells to detect cell proliferation, co-cultured supernatant cytokines and Tregs expression.
UNASSIGNED: The results indicate that the ITP patients showed higher expression of CD83 than the healthy controls. The proliferation of CD4+ T cells was inhibited by downregulation of DCs-CD83 but promoted by overexpression of DCs-CD83. siRNA-CD83 inhibited proinflammatory IFN-γ and IL-17 secretion while raising TGF-β, IL-10 concentrations. Overexpression of DCs-CD83 promoted Tregs expression.
UNASSIGNED: The Th1/Th2 and Th17/Tregs polarization were reversed via interfering DCs with siRNA-CD83. CD83 plays an important role in ITP pathogenesis, suggesting novel treatment for ITP patients.
摘要：
■CD83与免疫性血小板减少症(ITP)的发病机制密切相关,但确切的机制尚不清楚。
■探讨CD83与CD4+T细胞亚群的关系，阐明CD83在ITP发病中的作用。
RT-qPCR和流式细胞术用于说明CD83表达。下调和过表达DC-CD83与CD4+T细胞共培养,检测细胞增殖,共培养的上清液细胞因子和Tregs表达。
■结果表明ITP患者比健康对照显示更高的CD83表达。DC-CD83的下调抑制了CD4+T细胞的增殖，但DC-CD83的过表达促进了CD4+T细胞的增殖。siRNA-CD83抑制促炎IFN-γ和IL-17的分泌，同时提高TGF-β，IL-10浓度。DC-CD83的过表达促进了Tregs的表达。
■通过用siRNA-CD83干扰DC来逆转Th1/Th2和Th17/Tregs极化。CD83在ITP发病机制中起重要作用,提示ITP患者的新治疗方法。
■探讨CD83与CD4+T细胞亚群的关系，阐明CD83在ITP发病中的作用。
RT-qPCR和流式细胞术用于说明CD83表达。下调和过表达DC-CD83与CD4+T细胞共培养,检测细胞增殖,共培养的上清液细胞因子和Tregs表达。
■结果表明ITP患者比健康对照显示更高的CD83表达。DC-CD83的下调抑制了CD4+T细胞的增殖，但DC-CD83的过表达促进了CD4+T细胞的增殖。siRNA-CD83抑制促炎IFN-γ和IL-17的分泌，同时提高TGF-β，IL-10浓度。DC-CD83的过表达促进了Tregs的表达。
■通过用siRNA-CD83干扰DC来逆转Th1/Th2和Th17/Tregs极化。CD83在ITP发病机制中起重要作用,提示ITP患者的新治疗方法。
