Stat6 is required for mediating responses to IL-4 and for the development of Th2 cells
Stat6 is required for mediating responses to IL-4 and for the development of Th2 cells
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DOI：
10.1016/s1074-7613(00)80439-2
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发表时间：
1996-03-01
期刊：
影响因子：
32.4
通讯作者：
Grusby, MJ
中科院分区：
文献类型：
--
作者：
Kaplan, MH;Schindler, U;Grusby, MJ
白细胞介素 - 4（IL - 4）对细胞的刺激会导致多种信号通路的激活，其中之一涉及Stat6。我们通过在胚胎干细胞中进行基因打靶技术培育出了Stat6缺陷型小鼠，以确定这种转录因子在介导IL - 4生物学功能中的作用。IL - 4诱导的MHC II类抗原和IL - 4受体在细胞表面表达的增加完全被消除，并且来自Stat6缺陷型动物的淋巴细胞在受到IL - 4刺激时无法增殖。Stat6缺陷型B细胞在体内用抗IgD免疫后不会产生IgE。此外，Stat6缺陷型T淋巴细胞在受到IL - 4或IL - 13刺激时无法分化为Th2细胞。这些结果表明，尽管存在由IL - 4激活的多种信号通路，但Stat6对于淋巴细胞中介导对IL - 4的反应是必不可少的。
Interleukin-4 (IL-4) stimulation of cells leads to the activation of multiple signaling pathways, one of which involves State. We have generated State-deficient mice by gene targeting in embryonic stem cells to determine the role of this transcription factor in mediating the biologic functions of IL-4. IL-4-induced increases in the cell surface expression of both MHC class II antigens and IL-4 receptor are completely abrogated, and lymphocytes from State-deficient animals fail to proliferate in response to IL-4. Stat6-deficient B cells do not produce IgE following in vivo immunization with anti-IgD. In addition, State-deficient T lymphocytes fail to differentiate into Th2 cells in response to either IL-4 or IL-13. These results demonstrate that, despite the existence of multiple signaling pathways activated by IL-4, State is essential for mediating responses to IL-4 in lymphocytes.