Type I interferon: a new player in TNF signaling.

Current directions in autoimmunity Pub Date : 2010-01-01 Epub Date: 2010-02-18 DOI:10.1159/000289199
Anna Yarilina, Lionel B Ivashkiv
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引用次数: 59

Abstract

TNF and type I interferons (IFNs) are induced by microbial stimuli and mediate innate immune responses. They are also involved in the pathogenesis of chronic inflammatory diseases, such as rheumatoid arthritis and systemic lupus erythematosus. Activated macrophages are an important driving force of inflammatory reactions and one of the major producers of TNF in innate immunity and chronic inflammation. Despite the fact that cells at sites of damage are continuously exposed to both cytokines, little is known about mechanisms regulating TNF and type I IFN interactions during inflammation. In this review, we discuss the role of an IFN-beta-mediated autocrine loop in the regulation of gene expression program induced by TNF in myeloid cells.

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I型干扰素:TNF信号传导的新参与者。
TNF和I型干扰素(ifn)由微生物刺激诱导并介导先天免疫反应。它们还参与慢性炎性疾病的发病机制,如类风湿关节炎和系统性红斑狼疮。活化的巨噬细胞是炎症反应的重要驱动力,是先天免疫和慢性炎症中TNF的主要产生者之一。尽管损伤部位的细胞持续暴露于这两种细胞因子,但在炎症期间调节TNF和I型IFN相互作用的机制知之甚少。在这篇综述中,我们讨论了ifn - β介导的自分泌环在髓细胞TNF诱导的基因表达程序调控中的作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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