Tengvall Sara, Che Karlhans Fru, Lindén Anders
Institute of Medicine, University of Gothenburg, Gothenburg, Sweden.
J Innate Immun. 2016;8(1):15-22. doi: 10.1159/000434646. Epub 2015 Jul 21.
The production of interleukin (IL)-26 was initially attributed to T cells, and in particular to Th17 cells. However, more recent findings indicate IL-26 production in natural killer (NK) cells, macrophages and fibroblast-like cells as well. It is known that IL-26 binds to the IL-20R1/IL-10R2 receptor complex on certain target cells, where it causes specific intracellular signaling and the secretion of IL-1β, IL-8 and TNF-α. In line with this type of proinflammatory role, IL-26 also increases chemotaxis of human neutrophils. Interestingly, high levels of IL-26 are present even in normal human airways, and endotoxin exposure further enhances these levels; this indicates involvement in antibacterial host defense. Studies on acute inflammatory disorders are few but there are studies showing the involvement of IL-26 in rheumatoid arthritis and inflammatory bowel disease. In conclusion, IL-26 is emerging as a potentially important player in host defense and may also be a pathogenic factor in the chronic inflammatory disorders of humans.
白细胞介素(IL)-26的产生最初被认为源于T细胞,尤其是Th17细胞。然而,最近的研究结果表明,自然杀伤(NK)细胞、巨噬细胞和成纤维样细胞也能产生IL-26。已知IL-26可与某些靶细胞上的IL-20R1/IL-10R2受体复合物结合,进而引发特定的细胞内信号传导,并促使IL-1β、IL-8和TNF-α的分泌。与这种促炎作用一致,IL-26还可增强人类中性粒细胞的趋化性。有趣的是,即使在正常人类气道中也存在高水平的IL-26,内毒素暴露会进一步提高这些水平;这表明其参与了抗菌宿主防御。关于急性炎症性疾病的研究较少,但有研究表明IL-26参与了类风湿性关节炎和炎症性肠病。总之,IL-26正在成为宿主防御中一个潜在的重要因子,也可能是人类慢性炎症性疾病的致病因素。