【摘要】 肠黏膜慢性炎症损伤是炎症性肠病(IBD)的重要病变特点,研究表明白细胞介素23(IL-23)/IL-17炎症轴参与肠黏膜炎性损伤并参与IBD的发生、发展、治疗与转归。IL-23为IL-17重要上游分子,可促进Th17细胞活化、增殖和炎性细胞因子的分泌,并参与IBD病变局部中性粒细胞、单核巨噬细胞、调节性T细胞(Treg)和3型固有淋巴细胞(ILC3)等多种免疫细胞炎性应答过程。IBD病变局部IL-23和IL-17表达升高,其形成的IL-23/IL-17炎症轴一方面通过抑制Treg而破坏肠道免疫耐受微环境,另一方面可激活自身反应性T细胞应答加剧肠黏膜炎性病理损伤。尽管临床研究表明IL-23/IL-17为多种炎症相关疾病的治疗靶点,靶向阻断IL-23治疗IBD也初见成效,但动物实验表明阻断IL-17并未减轻IBD肠道炎症,因此,深入理解IL-17/IL-23炎症轴与IBD的关系对其治疗的研究十分必要。更多还原

【Abstract】 Chronic inflammatory damage of intestinal mucosa is an important characteristic of inflammatory bowel disease(IBD). Studies have shown that the interleukin 23(IL-23)/IL-17 axis is involved in intestinal mucosal inflammatory injury and plays a crucial role in the development and prognosis of IBD. IL-23 is one of the upstream molecules of IL-17, which can promote Th17 cell activation, proliferation and the secretion of inflammatory cytokines. Moreover, IL-23 is involved in the inflammatory response process of various immune cells such as neutrophils, macrophages, regulatory T cells(Tregs), the group 3 innate lymphocytes(ILC3) during IBD. Previous studies demonstrated that IL-23 and IL-17 increased in IBD, which lead to an imbalance between Tregs and auto-reactive T cells to exacerbate the inflammatory pathological damage of the intestinal mucosa. Notably, although IL-23/IL-17 is potential therapeutic target for inflammation-related diseases and anti-IL-23 strategies has proven to be effective in treating IBD, the strategy of blocking IL-17 to treat IBD has failed. Therefore, a deep understanding of the relationship between IL-17/IL-23 axis and IBD is necessary for the study of IBD treatment.更多还原