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Stat1α 表达参与了 γ 干扰素对 II 类反式激活因子和 II 类主要组织相容性复合体基因的诱导过程。

Stat1 alpha expression is involved in IFN-gamma induction of the class II transactivator and class II MHC genes.

作者信息

Lee Y J, Benveniste E N

机构信息

Department of Cell Biology, University of Alabama at Birmingham 35294, USA.

出版信息

J Immunol. 1996 Aug 15;157(4):1559-68.

PMID:8759739
Abstract

Class II MHC Ags are critical in the regulation of immune responses by presenting Ag to T lymphocytes, resulting in their activation and differentiation. Class II expression is rare in the normal central nervous system, but elevated expression on glial cells has been observed in several neurologic diseases. We have previously demonstrated that IFN-gamma-induced class II expression in glial cells involves activation of both tyrosine kinase and protein kinase C. IFN-gamma induces tyrosine phosphorylation of the tyrosine kinases Jak1 and Jak2 and of Stat1 alpha. In addition, IFN-gamma enhances expression of Stat1 alpha mRNA and protein. We utilized antisense oligonucleotides against Stat1 alpha to determine directly whether IFN-gamma-induced activation and/or enhancement of Stat1 alpha is involved in class II expression. Antisense oligonucleotides complementary to Stat1 alpha mRNA were introduced in CH235-MG astroglioma cells by transient transfection; such treatment inhibited both constitutive and IFN-gamma-enhanced expression of Stat1 alpha. IFN-gamma-induced class II MHC expression was also inhibited in cells exposed to Stat1 alpha antisense oligonucleotides. The fact that the class II promoter does not contain IFN-gamma-activated sequences for binding Stat1 alpha suggests that Stat1 alpha must activate another protein that is directly involved in class II expression. A likely candidate is the class II MHC transactivator (CIITA). IFN-gamma induction of CIITA mRNA was also inhibited in cells treated with antisense oligonucleotides against Stat1 alpha. These findings demonstrate that Stat1 alpha is involved in IFN-gamma induction of CIITA expression, resulting in class II MHC expression.

摘要

II类主要组织相容性复合体抗原(Class II MHC Ags)通过将抗原呈递给T淋巴细胞来调节免疫反应,从而导致T淋巴细胞的激活和分化,在免疫反应调节中至关重要。II类表达在正常中枢神经系统中很少见,但在几种神经系统疾病中已观察到神经胶质细胞上的表达升高。我们之前已经证明,干扰素-γ(IFN-γ)诱导神经胶质细胞中II类表达涉及酪氨酸激酶和蛋白激酶C的激活。IFN-γ诱导酪氨酸激酶Jak1和Jak2以及Stat1α的酪氨酸磷酸化。此外,IFN-γ增强Stat1α mRNA和蛋白的表达。我们利用针对Stat1α的反义寡核苷酸直接确定IFN-γ诱导的Stat1α激活和/或增强是否参与II类表达。通过瞬时转染将与Stat1α mRNA互补的反义寡核苷酸导入CH235-MG星形胶质瘤细胞;这种处理抑制了Stat1α的组成型表达和IFN-γ增强的表达。在暴露于Stat1α反义寡核苷酸的细胞中,IFN-γ诱导的II类主要组织相容性复合体表达也受到抑制。II类启动子不包含用于结合Stat1α的IFN-γ激活序列,这一事实表明Stat1α必须激活另一种直接参与II类表达的蛋白质。一个可能的候选者是II类主要组织相容性复合体反式激活因子(CIITA)。在用针对Stat1α的反义寡核苷酸处理的细胞中,IFN-γ诱导的CIITA mRNA也受到抑制。这些发现表明Stat1α参与IFN-γ诱导的CIITA表达,从而导致II类主要组织相容性复合体表达。

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