胸腺基质淋巴细胞生成素对小鼠巨噬细胞抗原提呈功能及炎性分泌功能的影响  

TSLP modulates antigen-presenting function and pro-inflammatory cytokines production in mice macrophages

作　　者：林静[1] 王磊[2,3] 苏又苏[2,3] 方红成[2,3] 李大主[1] 

机构地区：[1]华中科技大学同济医学院协和医院心内科,武汉430022 [2]深圳市第六人民医院(南山医院) [3]华中科技大学协和深圳医院,深圳518052

出　　处：《中国免疫学杂志》2012年第12期1063-1067,共5页Chinese Journal of Immunology

基　　金：国家自然科学基金资助项目(No.81170258)

摘　　要：目的:研究胸腺基质淋巴细胞生成素(TSLP)对小鼠巨噬细胞抗原提呈能力及炎性分泌功能的影响和可能作用机制。方法:分离野生型C57B小鼠及TSLPR基因敲除(TSLPR-/-)C57B小鼠腹腔巨噬细胞,给予TSLP进行刺激。采用流式细胞术检测巨噬细胞MHCⅡ、CD86的表达;采用实时定量PCR以及ELISA方法检测小鼠巨噬细胞内以及培养上清液炎症因子MCP-1、TNF-α和IL-10的表达。结果:与野生型对照组比较,野生型实验组小鼠巨噬细胞表面抗原提呈分子(MHCⅡ,CD86)表达明显升高,炎症因子MCP-1和TNF-α表达及分泌均增高,IL-10表达及分泌无明显变化;与TSLPR基因敲除对照组相比较,TSLPR基因敲除小鼠巨噬细胞经TSLP刺激后细胞表面抗原提呈分子(MHCⅡ,CD86)表达及炎症因子MCP-1、TNF-α和IL-10的表达及分泌均无明显变化;与野生型实验组相比较,TSLPR基因敲除可明显抑制TSLP诱导的小鼠巨噬细胞抗原提呈分子增加以及炎症因子表达。结论:TSLP可通过与TSLPR结合促进小鼠巨噬细胞活化,增加巨噬细胞抗原递呈能力,产生炎症因子,促使小鼠巨噬细胞向促炎巨噬细胞表型M1型转化。Objective：To investigate the effect and mechanism of TSLP modulating antigen-presenting function and pro-inflammatory cytokines production in mice macrophages.Methods：Peritoneal macrophages were isolated and collected from wild C57BL mice or TSLPR knockdown mice.Then,cells were cultured with PBS or stimulated with TSLP.Flow cytometry was used to determine the phenotyoe of macrophages.RT-PCR and ELISA were used to measure MCP-1,TNF-α and IL-10 production.Results：Upon stimulated with TSLP,peritoneal macrophages from wild mice exhibited up-regulated MHCⅡ and CD86 expression,and increased pro-inflammatory cytokine,MCP-1 and TNF-α production.Compared with unstimulated cells,however,peritoneal macrophages from TSLRP knockdown mice had no changes in MHCⅡ and CD86 expression,and in pro-inflammatory cytokine production responding to TSLP.Under stimulated with TSLP,macrophages from TSLPR knockdown mice showed decreased MHCⅡ and CD86 expression and pro-inflammatory cytokines production compared to which from wild mice.Conclusion：Results collectively suggest that via binding to TSLPR,TSLP could facilitate mice macrophage antigen-presenting function and steer macrophage differentiation toward an pro-inflammatory cytokine producing phenotype.

关 键 词：TSLP TSLPR基因敲除 小鼠巨噬细胞 抗原提呈能力 炎症因子 

分 类 号：R392.12[医药卫生—免疫学]