Steinert Anna, Linas Ioannis, Kaya Berna, Ibrahim Mohamed, Schlitzer Andreas, Hruz Petr, Radulovic Katarina, Terracciano Luigi, Macpherson Andrew J, Niess Jan Hendrik
Division of Gastroenterology and Hepatology, University Hospital Basel, 4031 Basel, Switzerland.
Department of Biomedicine, University of Basel, 4031 Basel, Switzerland.
J Immunol. 2017 Oct 1;199(7):2570-2584. doi: 10.4049/jimmunol.1700350. Epub 2017 Sep 1.
IL-19, a member of the IL-10 cytokine family that signals through the IL-20 receptor type I (IL-20Rα:IL-20Rβ), is a cytokine whose function is not completely known. In this article, we show that the expression of in biopsies of patients with active ulcerative colitis was increased compared with patients with quiescent ulcerative colitis and that colitis was attenuated in IL-19-deficient mice. The disruption of the epithelial barrier with dextran sodium sulfate leads to increased IL-19 expression. Attenuated colitis in IL-19-deficient animals was associated with reduced numbers of IL-6-producing macrophages in the inflamed colonic lamina propria. Microbial-driven expression of IL-19 by intestinal macrophages may contribute to the pathogenesis of inflammatory bowel disease.
白细胞介素-19（IL-19）是白细胞介素-10细胞因子家族的成员，通过I型白细胞介素-20受体（IL-20Rα:IL-20Rβ）发出信号，是一种功能尚未完全明确的细胞因子。在本文中，我们发现，与静止期溃疡性结肠炎患者相比，活动期溃疡性结肠炎患者活检组织中IL-19的表达增加，并且在IL-19基因敲除小鼠中结肠炎得到缓解。用葡聚糖硫酸钠破坏上皮屏障会导致IL-19表达增加。IL-19基因敲除动物中结肠炎的缓解与炎症性结肠固有层中产生IL-6的巨噬细胞数量减少有关。肠道巨噬细胞由微生物驱动表达IL-19可能参与炎症性肠病的发病机制。
