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目的 :观察Toll样受体7(Toll like receptor 7,TLR7)激动剂Imiquimod对白细胞介素10(interleukin 10,IL-10)转染小鼠骨髓来源的树突状细胞(bone-marrow derived dendritic cell,mDC)免疫功能影响。方法:转染IL-10至小鼠m DC,TLR7激动剂Imiquimod刺激48 h,利用流式细胞仪检测DC表面标志MHCⅡ、CD80、CD86及Fas L等分子的表达;ELISA检测细胞产生IL-6、肿瘤坏死因子α(TNF-α)。结果 :IL-10抑制m DC表达MHCⅡ、CD80、CD86分子,降低其分泌IL-6、TNF-α,促进其表达Fas L,而TLR7激动剂刺激增加了IL-10转染m DC表达MHCⅡ、CD80、CD86分子,促进其产生IL-6、TNF-α,抑制Fas L表达。结论:TLR7激动剂可逆转IL-10诱发的DC免疫应答低下。
OBJECTIVE: To observe the effect of interleukin 10 (IL-10) transfected mouse bone marrow-derived dendritic cells (IMLs) derived from Toll-like receptor 7 (TLR7) agonist Imiquimod , mDC) Immune function. Methods: The expression of MHCⅡ, CD80, CD86 and Fas L were detected by flow cytometry after transfection of IL-10 to mouse m DC and TLR7 agonist Imiquimod. IL-6 , Tumor necrosis factor alpha (TNF-alpha). Results: IL-10 inhibited the expression of MHCⅡ, CD80 and CD86 in m DC, decreased the secretion of IL-6 and TNF-α and promoted the expression of Fas L, while TLR7 agonist increased the expression of MHCⅡ in m DC by IL- CD80, CD86 molecules to promote their production of IL-6, TNF-α, inhibit Fas L expression. Conclusion: TLR7 agonists can reverse the low immune response induced by IL-10.