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IL-6负调控TH1细胞分化的分子机制

IL-6 Down-regulate the Differential development of TH1 Cell
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摘要 T_H细胞分化为T_H1和T_H2细胞亚群是受多种细胞因子调控的。已有研究资料表明:IL-6可启动CD4^+T_H2的分化,但新近发现IL-6由于可上调CD4^+T细胞SOCS-1基因的表达,干扰了IFNγ受体的信号转导,从而阻断了IFNγ对IFNγ基因的自我调节,因此实现了IL-6对T_H1细胞的负性调控。据此认为IL-6启动CD_4^+T_H2细胞分化与抑制CD_4^+T分化为T_H1细胞是两种独立的分子机制,它在平衡T_H1/T_H2的免疫反应中起着重要的调节作用。 TH cells differentiation to TH1 and TH2 sub - sets is controlled by several cytokines. IL- 6 can start the differen-tiation of CD_4^+ TH2 cell; but IL - 6 can up - regulate the expression of gene SOCS-1, disturb the signal transduction of IFN-γreceptor, and block the self - regulation of IFN -γ on its own gene. So there should be two independent pathways for IL -6 to play roles in CD_4^+ T cell: starting the differentiation to TH2 cell and suppressing the differentiation to TH1.
作者 吴翰桂 骆大法
机构地区 台州学院生物系 台州学院
出处 《台州学院学报》 2002年第6期68-70,共3页 Journal of Taizhou University
关键词 TH IL-6 信号传导 STAT SOCS TH IL-6 signal transduction STAT SOCS
分类号 R392 [医药卫生—免疫学]
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参考文献10

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台州学院学报
2002年 第6期

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