Yarilina Anna, Ivashkiv Lionel B
Arthritis and Tissue Degeneration Program, Hospital for Special Surgery, 535 East 70th Street, New York, NY 10021, USA.
Curr Dir Autoimmun. 2010;11:94-104. doi: 10.1159/000289199. Epub 2010 Feb 18.
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.
肿瘤坏死因子（TNF）和I型干扰素（IFN）由微生物刺激诱导产生，并介导先天性免疫反应。它们还参与慢性炎症性疾病的发病机制，如类风湿性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，也是先天性免疫和慢性炎症中TNF的主要产生者之一。尽管受损部位的细胞持续暴露于这两种细胞因子，但关于炎症期间调节TNF和I型干扰素相互作用的机制却知之甚少。在这篇综述中，我们讨论了IFN-β介导的自分泌环在调节髓系细胞中TNF诱导的基因表达程序中的作用。
