SIGNALING VIA MHC CLASS-II MOLECULES SELECTIVELY INDUCES IL-1-BETA OVER IL-1 RECEPTOR ANTAGONIST GENE-EXPRESSION

SIGNALING VIA MHC CLASS-II MOLECULES SELECTIVELY INDUCES IL-1-BETA OVER IL-1 RECEPTOR ANTAGONIST GENE-EXPRESSION
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DOI:
10.1006/bbrc.1994.1779
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发表时间:
1994-06-15
影响因子:
3.1
通讯作者:
MOURAD, W
MOURAD, W
中科院分区:
生物学4区
文献类型:
--
作者:
ALDACCAK, R;MEHINDATE, K;MOURAD, W

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几种类型的刺激对人单核细胞或人单核细胞系的激活协同诱导IL-1β及其拮抗剂(IL-1Ra)基因表达;它们平衡的改变似乎介导了炎症反应。使用人单核细胞系 THP-1,我们报告超级抗原,例如葡萄球菌肠毒素 A (SEA) 和关节炎支原体衍生的超级抗原 (MAM) 会诱导 IL-1 β mRNA 水平增加,但对 IL-1Ra mRNA 没有任何可检测到的影响。与 MAM 诱导的 IL-1 β mRNA 不同,SEA 诱导的 IL-1 β mRNA 被充分翻译成蛋白质。超抗原诱导的基因表达是通过其受体、MHC II 类分子的信号传导介导的。因此,这种信号传导模式似乎选择性诱导促炎细胞因子IL-1β基因表达,其本身在疾病病理学尤其是自身免疫性疾病中具有重要意义。 (C) 1994 年学术出版社
Activation of human monocytes or human monocytic cell lines by several types of stimuli coordinately induces IL-1 beta and its antagonist (IL-1Ra) gene expression; alterations in their balance seem to mediate the inflammatory response. Using the human monocytic cell line THP-1, we report that superantigens, such as staphylococcal enterotoxin A (SEA) and Mycoplasma arthritidis-derived superantigen (MAM) induce an increase in the level of IL-1 beta mRNA without any detectable effect on IL-1Ra mRNA. Unlike MAM-induced IL-1 beta mRNA, SEA-induced IL-1 beta mRNA was adequatly translated into protein. Superantigen-induced gene expression is mediated by signalling, via their receptors, the MHC class II molecules. Thus, it appears that this mode of signalling selectively induces the proinflammatory cytokine IL-1 beta gene expression which, by itself, can have major importance in disease pathology especially in autoimmune diseases. (C) 1994 Academic Press, Inc.