摘要
目的:研究Sel1L(Suppressor/enhancer of Lin-12-like)基因对小鼠骨髓源树突状细胞(BMDCs)分化及其功能的影响。方法:利用Cre-Loxp重组系统构建Sel1L基因敲除小鼠模型,用ELISA和实时荧光定量法检测BMDCs分泌细胞因子IL-6、IL-12的表达;用免疫印迹法(Western bolt)检测BMDCs细胞中Sel1L蛋白的表达;用流式细胞术检测BMDCs细胞CFSE、细胞表面分子CD80、CD86、MHC-Ⅰ、MHC-Ⅱ及其对特异性CD4^+T细胞抗原提呈能力的影响。结果:Sel1L的缺失抑制BMDC诱导分化过程中的增殖效率,上调DCs分泌因子的能力和MHC-Ⅰ的表达,减少MHC-Ⅱ的表达,并抑制BMDCs细胞对OVA_(323-339)抗原特异性T细胞的增殖。结论:Sel1L缺失可以抑制小鼠骨髓源树突状细胞的分化,下调DC对OVA特异性的CD4^+T细胞的抗原提呈功能。
Objective：To explore the effects of suppress or enhancer of lin-12-like（Sel1L）on differentiation and function of bone marrow-derived dendritic cells.Methods：To generate conditional knockout mice by the Cre-Loxp recombination system.ELISA and Real-time fluorescence quantitative PCR（RT-PCR）was used for analyzing the protein levels and mRNA levels of IL-6/IL-12 in BMDCs.The protein levels of Sel1L in BMDCs were detected by Western bolt.The expression of CFSE,CD80,CD86,MHC-Ⅰ,MHC-Ⅱon BMDCs and the capability in priming OVA specific CD4~＋T cells proliferation were analyzed by the flow cytometry.Results：The deficiency of Sel1L decreases the proliferation of DCs during its differentiation,up-regulates the secretion of IL-6,IL-12 and the expression of MHC-Ⅰ.Notably,Sel1L-null DCs was failed to up-regulate MHC-Ⅱexpression and dramatically impaired their ability to prime OVA_（323-339）specific CD4~＋T cell.Conclusion：The deletion of Sel1L can reduce the proliferation of BMDCs and down-regulate its ability in priming the proliferation of OVA specific CD4~＋T cells.
作者
许洁
颜楠楠
赵传祥
李慈
吴仪
肖腾飞
高凤威
周文慧
邵启祥
龙乔明
夏圣
XU Jie;YAN Nan-Nan;ZHAO Chuan-Xiang;LI Ci;WU Yi;XIAO Teng-Fei;GAO Feng-Wei;ZHOU Wen-Hui;SHAO Qi-Xiang;LONG Qiao-Ming;XIA Sheng(Department of Immunology, School of Medicine, Jiangsu University, Zhenjiang 212013, China)
出处
《中国免疫学杂志》
CAS
CSCD
北大核心
2018年第5期727-731,共5页
Chinese Journal of Immunology
基金
国家自然科学基金(31570879
31428006)
江苏省社会发展重点项目(BE2017696)资助
