论文部分内容阅读
克罗恩氏病与溃疡性结肠炎是两类临床上常见的炎症反应(immune bowel disease),主要表现为对肠道微生物异常的免疫反应。IL-1家族的细胞因子在炎症反应部位表达量都会上调,并促进炎症的恶化。然而,缺乏IL-1beta或IL-18的小鼠却表现出对DSS诱导的肠炎更为敏感的特性。因此,IL-1家族的蛋白对肠炎的发病具有复杂的调控作用。之前的研究证明IL-36家族的蛋白从属于IL-1蛋白家族,而对于这一类蛋白在肠炎中的作用却很少有研究。最近,来自佐治亚州立大学的Timothy L.Denning在《jounral of immunology》杂志上发表文章揭示了细胞因子IL-36 gamma在
Crohn’s disease and ulcerative colitis are two types of clinically common inflammatory bowel disease, mainly manifested as an abnormal immune response to gut microbes. IL-1 family of cytokines in the expression of inflammatory response sites will be increased, and promote the deterioration of inflammation. However, mice lacking IL-1beta or IL-18 exhibited more susceptible properties to DSS-induced enteritis. Therefore, the IL-1 family of proteins has a complex regulatory role in the pathogenesis of enteritis. Previous studies have demonstrated that the IL-36 family of proteins is subordinate to the IL-1 family of proteins and few studies have investigated the role of this class of proteins in enteritis. Recently, an article published in the journal “Journal of Immunology” by Timothy L. Denning from Georgia State University revealed that the cytokine IL-36 gamma