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分化的2型辅助性T细胞中白细胞介素-4和白细胞介素-13的产生不依赖于白细胞介素-4。

IL-4 and IL-13 production in differentiated T helper type 2 cells is not IL-4 dependent.

作者信息

Huang H, Hu-Li J, Chen H, Ben-Sasson S Z, Paul W E

机构信息

Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892-1892, USA.

出版信息

J Immunol. 1997 Oct 15;159(8):3731-8.

PMID:9378959
Abstract

CD4+ T cell differentiation into cells capable of producing IL-4 and IL-13 (Th2 cells) requires the presence of IL-4 and is STAT-6 dependent. Here we show that IL-4 is not required for IL-4 or IL-13 production by Th2 cells. Anti-IL-4 or anti-IL-4R Ab did not diminish IL-4 production by Th2 cells in response to TCR-mediated stimulation, nor did IL-4 enhance IL-4 production in response to stimulation of Th2 cells with limiting amounts of Ag. Th2 cells prepared from IL-4 knockout mice were capable of producing IL-13 mRNA in response to stimulation with immobilized anti-CD3. IL-4 did not increase IL-13 mRNA expression. Despite the failure of IL-4 to effect IL-4 production by primed Th2 cells, a STAT-6 binding element was demonstrated in the IL-4 promoter. The authenticity of this element was demonstrated by oligonucleotide competition, by supershifting with anti-STAT-6 Ab, and by IL-4-inducible effects on transcription of a reporter gene under the control of a multimerized element fused to an IL-4 minimal promoter. Nonetheless, an IL-4 promoter construct lacking the STAT-6 binding element was as effective as a construct containing this element in anti-CD3-induced reporter transcription. Thus, this element, if biologically active, must function at a step in T cell responsiveness distinct from the acute production of IL-4 by Th2 cells in response to Ag or anti-CD3.

摘要

CD4 + T细胞分化为能够产生白细胞介素-4(IL-4)和白细胞介素-13(IL-13)的细胞(Th2细胞)需要IL-4的存在,并且依赖于信号转导和转录激活因子6(STAT-6)。在此我们表明,Th2细胞产生IL-4或IL-13并不需要IL-4。抗IL-4或抗IL-4受体抗体不会减少Th2细胞因T细胞受体介导的刺激而产生的IL-4,在用限量抗原刺激Th2细胞时,IL-4也不会增强IL-4的产生。从IL-4基因敲除小鼠制备的Th2细胞能够在固定化抗CD3刺激下产生IL-13信使核糖核酸(mRNA)。IL-4不会增加IL-13 mRNA的表达。尽管IL-4无法影响已致敏Th2细胞产生IL-4,但在IL-4启动子中证实存在一个STAT-6结合元件。通过寡核苷酸竞争、用抗STAT-6抗体进行超迁移以及IL-4对与IL-4最小启动子融合的多聚化元件控制下的报告基因转录的诱导作用,证明了该元件的真实性。然而,在抗CD3诱导的报告基因转录中,缺少STAT-6结合元件的IL-4启动子构建体与含有该元件的构建体一样有效。因此,该元件如果具有生物学活性,必定在T细胞反应性的一个步骤中发挥作用,该步骤不同于Th2细胞在响应抗原或抗CD3时急性产生IL-4的过程。

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