Kuwabara Taku, Ishikawa Fumio, Kondo Motonari, Kakiuchi Terutaka
Department of Molecular Immunology, Toho University School of Medicine, Tokyo 143-8540, Japan.
Mediators Inflamm. 2017;2017:3908061. doi: 10.1155/2017/3908061. Epub 2017 Feb 20.
Interleukin-17 (IL-17) induces the production of granulocyte colony-stimulating factor (G-CSF) and chemokines such as CXCL1 and CXCL2 and is a cytokine that acts as an inflammation mediator. During infection, IL-17 is needed to eliminate extracellular bacteria and fungi, by inducing antimicrobial peptides such as defensin. This cytokine also plays an important role in chronic inflammation that occurs during the pathogenesis of autoimmune diseases and allergies such as human rheumatoid arthritis (RA) for which a mouse model of collagen-induced arthritis (CIA) is available. In autoimmune diseases such as RA and multiple sclerosis (MS), IL-17 is produced by helper T (Th) cells that are stimulated by IL-1 and IL-6 derived from phagocytes such as macrophages and from tissue cells. IL-17 contributes to various lesions that are produced by Th17 cells, one subset of helper T cells, and by T cells and innate lymphoid cells. It strongly contributes to autoimmune diseases that are accompanied by chronic inflammation. Thus, a functional understanding of Th17 cells is extremely important. In this review, we highlight the roles of cytokines that promote the development and maintenance of pathogenic Th17 cells in autoimmune diseases.
白细胞介素-17（IL-17）可诱导粒细胞集落刺激因子（G-CSF）以及趋化因子如CXCL1和CXCL2的产生，是一种作为炎症介质的细胞因子。在感染期间，需要IL-17通过诱导防御素等抗菌肽来清除细胞外细菌和真菌。这种细胞因子在自身免疫性疾病和过敏（如人类类风湿性关节炎（RA））发病机制中发生的慢性炎症中也起重要作用，针对RA有胶原诱导性关节炎（CIA）的小鼠模型。在诸如RA和多发性硬化症（MS）等自身免疫性疾病中，IL-17由辅助性T（Th）细胞产生，这些Th细胞受到来自吞噬细胞（如巨噬细胞）和组织细胞的IL-1和IL-6的刺激。IL-17促成了由辅助性T细胞的一个亚群Th17细胞以及T细胞和天然淋巴细胞产生的各种损伤。它对伴有慢性炎症的自身免疫性疾病有很大影响。因此，对Th17细胞的功能理解极其重要。在本综述中，我们重点介绍了在自身免疫性疾病中促进致病性Th17细胞发育和维持的细胞因子的作用。
