Let-7i靶向抑制SOCS1调控树突状细胞功能  

Let-7i regulates DCs functional status by translationally suppression of SOCS1

作　　者：张毛毛[1] 黄兴涛[1] 张露露[1] 张若溪[1] 吴健[1] 于波[1] 

机构地区：[1]哈尔滨医科大学附属第二医院心内科,省部共建心肌缺血诊疗重点实验室,150081

出　　处：《免疫学杂志》2015年第9期737-741,共5页Immunological Journal

基　　金：黑龙江省教育厅面上项目(12531286)

摘　　要：目的探讨microRNA let-7i调控树突状细胞(DC)功能的作用靶点。方法分别上调或下调DC中let-7i水平,应用双萤光素酶报告基因系统检测SOCS1是否是let-7i的作用靶点,应用Western blot及免疫荧光检测DC中SOCS1蛋白水平,qRTPCR检测DC中SOCS1及let-7i基因水平,观察在调控DC功能的过程中,let-7i是否靶向抑制SOCS1表达。结果 let-7i通过转录后抑制的方式靶向调控DC中SOCS1表达。结论 miRNA let-7i靶向抑制SOCS1,进而影响DC的成熟及功能状态。Dendritic cells （DCs） can initiate immune responses or confer immune tolerance depending on functional status. MicroRNAs are critical for the regulation of DC function and immunity, and microRNA let-7i was upregulated during LPS-induced DC maturation. Previous studies showed that downregulation of let-7i significantly impeded DC maturation and functional status. In this study, the target of let-7i was explored. Suppressor of cytokine signaling 1 （SOCS1）, a crucial mediator of DC maturation, was confirmed as a let-7i target gene by luciferase construct assay. Suppression or overexpression of let-7i caused reciprocal alterations in SOCS1 protein expression, but had no significant effects on SOCS1 mRNA levels, indicating that let-7i regulated SOCS1 expression by translational suppression. The modulation of SOCS1 protein by let-7i was mainly restricted to CD86-DCs. Our study demonstrates that let-7i regulation of SOCS1 is critical for LPS-induced DC maturation and immune function. Dynamic regulation of let-7i may fine-tune immune responses by inducing Ag-specific immune tolerance.

关 键 词：miRNA let-7i 树突状细胞 免疫调控 SOCS1 

分 类 号：R392[医药卫生—免疫学]