| 注册
首页|期刊导航|重庆医学|SOCS3基因转染对小鼠CD4+T h细胞分化及炎症细胞因子表达的影响及机制研究

SOCS3基因转染对小鼠CD4+T h细胞分化及炎症细胞因子表达的影响及机制研究

张沛 董念国 刘金平

重庆医学2016,Vol.45Issue(36):5049-5051,5055,4.
重庆医学2016,Vol.45Issue(36):5049-5051,5055,4.DOI:10.3969/j.issn.1671-8348.2016.36.003

SOCS3基因转染对小鼠CD4+T h细胞分化及炎症细胞因子表达的影响及机制研究

The effects and mechanism of SOCS3 gene transfection in CD4+Th cell differentiation and expression of inflammatory cytokines of mouse

张沛 1董念国 2刘金平2

作者信息

  • 1. 重庆医科大学附属第二医院胸心外科 400010
  • 2. 华中科技大学同济医学院附属协和医院心脏大血管外科,武汉410030
  • 折叠

摘要

Abstract

Objective To investigate the effect and mechanism of adenovirus vector mediated SOCS 3 gene transfection in CD4+ Th cell differentiation and expression of inflammatory cytokines of mouse .Methods The CD4+ Th cells were isolated from spleen of C57bl/6 mouse and cultured .Ad‐SOCS3 were transfected into the CD4+ Th cells .PHA was used for culturing with the CD4+ Th cells .RT‐PCR were used to detect the mRNA expression ,and Western blot were used to detect the protein expression of cytokines .Results Compared with the control group ,the gene and protein expression of T‐bet ,IL‐2 ,IFN‐γ,STAT4 and IL‐12Rβ2 in the transfected group were significantly down‐regulated ,the gene and protein expression of SOCS3 ,GATA‐3 ,IL‐4 ,IL‐6 ,IL‐10 and STAT6 were significantly up‐regulated(P<0 .01) .Conclusion The results indicate that SOCS3 gene transfection can up‐regu‐late SOCS3 mRNA and protein expression in the CD4+ Th cells ,down‐regulate the JAK/STAT pathway ,inhibition of Th1 cell dif‐ferentiation ,and down regulation of inflammatory cytokine gene and protein expression ,and indirectly promote Th2 cell differentia‐tion ,and up the corresponding inflammatory cytokine gene and protein expression .

关键词

T淋巴细胞,辅助诱导/细胞因子信号转导蛋白抑制因子/细胞分化/细胞因子类

Key words

T-lymphocytes ,helper-inducer/suppressor of cytokine signaling proteins/cell differentiation/cytokines

分类

医药卫生

引用本文复制引用

张沛,董念国,刘金平..SOCS3基因转染对小鼠CD4+T h细胞分化及炎症细胞因子表达的影响及机制研究[J].重庆医学,2016,45(36):5049-5051,5055,4.

基金项目

国家自然科学基金资助项目(81270322)。 ()

重庆医学

OA北大核心

1671-8348

访问量0
|
下载量0
段落导航相关论文