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首页> 外文期刊>Cellular Signalling >Interleukin-1 regulates keratinocyte expression of T cell targeting chemokines through interleukin-1 receptor associated kinase-1 (IRAK1) dependent and independent pathways
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Interleukin-1 regulates keratinocyte expression of T cell targeting chemokines through interleukin-1 receptor associated kinase-1 (IRAK1) dependent and independent pathways

机译：白介素-1通过白介素-1受体相关激酶1（IRAK1）依赖和独立途径调节靶向T细胞的趋化因子的角质形成细胞表达。

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摘要

IL-1 is a potent pro-inflammatory cytokine that activates intracellular signaling cascades some of which may involve IL-1 receptor associated kinase-1 (IRAK1). Psoriasis is a T cell dependent chronic inflammatory condition of the skin of unknown cause. IL-1 has been implicated in psoriasis pathology, but the mechanism has not been elucidated. Interestingly, expression of IRAK1 is elevated in psoriatic skin. To identify a potential link between IL-1, keratinocytes and T cells in skin inflammation we employed pathway-focused microarrays to evaluate IL-1 dependent gene expression in keratinocytes. Several candidate mRNAs encoding known T cell chemoattractants were identified in primary keratinocytes and the stable keratinocyte cell line HaCaT. CCL5 and CCL20 mRNA and protein levels were confirmed up-regulated by IL-1 in concentration and time-dependent manners. Furthermore IL-1 synergized with IFN-gamma and TNF-alpha. Expression of CXCL9, CXCL10 and CXCL11 mRNAs was also increased in response to IL-1, but protein could only be detected in medium from cells treated with IFN-gamma alone or in combination with IL-1. Over-expression of IRAK1 led to increased constitutive and cytokine induced production of CCL5 and CCL20. Inhibition of IRAK1 activity through RNAi or expression of a dominant negative mutant blocked production of CCL5 and CCL20 but had no effect upon the IL-1 enhancement of IFN-gamma induced CXCL9, CXCL10 and CXCL11 production. In conclusion IL-1 regulates T cell targeting chemokine production in keratinocytes through IRAK1 dependent and independent pathways. These pathways may contribute to acute and chronic skin inflammation.
机译：IL-1是一种有效的促炎细胞因子，可激活细胞内信号传导级联反应，其中一些可能涉及IL-1受体相关激酶1（IRAK1）。牛皮癣是原因不明的皮肤的T细胞依赖性慢性炎症。 IL-1与牛皮癣的病理学有关，但其机理尚未阐明。有趣的是，IRAK1的表达在牛皮癣皮肤中升高。为了确定皮肤炎症中IL-1，角质形成细胞和T细胞之间的潜在联系，我们采用了以途径为重点的微阵列来评估角质形成细胞中IL-1依赖性基因的表达。在原代角质形成细胞和稳定的角质形成细胞系HaCaT中鉴定了几种编码已知T细胞趋化因子的候选mRNA。 IL-1以浓度和时间依赖性方式证实CCL5和CCL20的mRNA和蛋白质水平上调。此外，IL-1与IFN-γ和TNF-α协同作用。响应IL-1，CXCL9，CXCL10和CXCL11 mRNA的表达也增加，但仅在单独用IFN-γ或与IL-1联合处理的细胞的培养基中才能检测到蛋白质。 IRAK1的过表达导致组成型和细胞因子诱导的CCL5和CCL20产生增加。通过RNAi抑制IRAK1活性或显性负突变体的表达可阻止CCL5和CCL20的产生，但对IFN-γ诱导的CXCL9，CXCL10和CXCL11产生的IL-1增强没有影响。总之，IL-1通过IRAK1依赖性和非依赖性途径调节角质形成细胞中T细胞靶向趋化因子的产生。这些途径可能导致急性和慢性皮肤炎症。

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