Kurimoto Masayuki, Watanabe Tomohiro, Kamata Ken, Minaga Kosuke, Kudo Masatoshi
Department of Gastroenterology and Hepatology, Kindai University Faculty of Medicine, Osakasayama, Japan.
Front Physiol. 2021 Oct 25;12:781012. doi: 10.3389/fphys.2021.781012. eCollection 2021.
IL-33 is a pleiotropic cytokine that promotes inflammation and fibrosis. IL-33 is produced by a broad range of cells, including antigen-presenting cells (APCs), epithelial cells, and fibroblasts. IL-33 produced by the innate immune cells has been shown to activate pro-inflammatory T helper type 1 (Th1) and T helper type 2 (Th2) responses. The intestinal barrier and tolerogenic immune responses against commensal microbiota contribute to the maintenance of gut immune homeostasis. Breakdown of tolerogenic responses against commensal microbiota as a result of intestinal barrier dysfunction underlies the immunopathogenesis of inflammatory bowel diseases (IBD) and pancreatitis. Recent studies have provided evidence that IL-33 is an innate immune cytokine that bridges adaptive Th1 and Th2 responses associated with IBD and pancreatitis. In this Mini Review, we discuss the pathogenic roles played by IL-33 in the development of IBD and pancreatitis and consider the potential of this cytokine to be a new therapeutic target.
白细胞介素-33（IL-33）是一种多效性细胞因子，可促进炎症和纤维化。包括抗原呈递细胞（APC）、上皮细胞和成纤维细胞在内的多种细胞均可产生IL-33。固有免疫细胞产生的IL-33已被证明可激活促炎性1型辅助性T细胞（Th1）和2型辅助性T细胞（Th2）反应。肠道屏障以及针对共生微生物群的耐受性免疫反应有助于维持肠道免疫稳态。由于肠道屏障功能障碍导致针对共生微生物群的耐受性反应破坏，是炎症性肠病（IBD）和胰腺炎免疫发病机制的基础。最近的研究提供了证据，表明IL-33是一种固有免疫细胞因子，它在与IBD和胰腺炎相关的适应性Th1和Th2反应之间起桥梁作用。在本综述中，我们讨论了IL-33在IBD和胰腺炎发生发展中所起的致病作用，并考虑了这种细胞因子作为新治疗靶点的潜力。
