摘要
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 effects of TLR7 agonist on the immune function of IL-10 transfected bone-marrow derived dendritic cell(m DC). Methods:The IL-10 plasmid was transfected to mouse m DC,and TLR7 agonist,Imiquimod,was added to m DC for 48 h. The expression of MHCⅡ,CD80,CD86,Fas L in m DC were detected with flow cytometry,and the production of the IL-6 and TNF-α was detemined by ELISA. Results:IL-10 suppressed the expression of MHCⅡ,CD80,CD86,decreased the production of IL-6and TNF-α,and increased the expression of Fas L on m DC. Imiquimod increased the expression of MHC Ⅱ,CD80 and CD86,which enhanced the production of IL-6 and TNF-α,but inhibited of Fas L expression by the IL-10 transfected m DC. Conclusion:TLR7activation reverses IL-10 induced low response of m DC.
出处
《南京医科大学学报(自然科学版)》
CAS
CSCD
北大核心
2015年第10期1360-1363,共4页
Journal of Nanjing Medical University(Natural Sciences)
基金
广东省科技计划项目(2013B060300012
2014A030304024)
南方医院院长基金(201213006)