TLR2激动剂Pam3CK逆转IL-10转染小鼠髓样树突状细胞免疫功能的研究  

TLR2 agonist Pam3CK reverses the immune function of the IL-10 transfected mouse bone marrow-derived dendritic cells

作　　者：张志丽[1] 吴砂[1] 卢晓[1] 弓莉[2] 富宁[1] 

机构地区：[1]南方医科大学基础医学院免疫教研室,广州510515 [2]南方医科大学南方医院实验动物研究中心,广州510515

出　　处：《中国免疫学杂志》2011年第4期300-302,307,共4页Chinese Journal of Immunology

基　　金：国家自然基金资助项目(C080701)

摘　　要：目的:观察TLR2激活剂Pam3CK对IL-10转染小鼠髓样树突状细胞免疫功能影响。方法:转染IL-10至小鼠髓样树突状细胞(mDC),TLR2配体Pam3CK刺激48小时,利用流式细胞仪检测DC表面标志MHCⅡ、CD80、CD86及FasL等分子的表达;ELISA检测细胞产生IL-6、TNF-α。结果:IL-10抑制mDC表达CD80、CD86、MHCⅡ类分子,降低其分泌IL-6、TNF-α,促进其表达FasL,而TLR2激动剂刺激增加了IL-10转染DC表达MHC-Ⅱ类分子及CD80、CD86,促进其产生IL-6及TNF-α,抑制了FasL表达。结论:TLR2激动剂可逆转IL-10诱发的DC免疫应答低下。Objective：The effects of TLR2 agonist on the immune function of IL-10 transfected bone-marrow derived dendritic cell（mDC）.Methods：The IL-10 plasmid was transfected to mouse mDC,and TLR2 agonist Pam3CK was added to mDC for 48 hrs.The expression of MHCⅡ,CD80,CD86,FasL in mDC was detected with flow cytometry,and the production of the IL6 and TNF-α was determined by ELISA.Results：IL-10 suppressed the expression of CD80,CD86 and MHCⅡ,decreased the production of IL-6,TNFα,and increased the expression of FasL on mDC.TLR2 agonist Pam3CK increased the expression of MHCⅡ,CD80 and CD86,enhanced the production of IL-6 and TNF-α,but inhibited of FasL expression by the IL-10 transfected mDC.Conclusion：TLR2 activation reverses IL-10 induced low-response of mDC.

关 键 词：IL-10 树突状细胞 TLR2激动剂 

分 类 号：R392[医药卫生—免疫学]