Th17细胞是CD4~+T细胞亚型之一,可分泌IL-17等炎性因子,诱导机体多种疾病。幽门螺旋杆菌(Helicobacter pylori,Hp)感染后,Cag A及Ure B等可影响Th17细胞数量,其机制可能与被感染的巨噬细胞直接诱导细胞分化、激活MyD88等信号通路及趋化因子的趋动有关,最终Th17、Treg细胞数量均较感染前增多,Th17/Treg平衡紊乱,总体向Treg漂移;同时,增多的Th17细胞一方面可通过募集中性粒细胞等参与Hp的清除,另一方面又扩大炎症反应,引起黏膜损伤甚至诱导癌变,从而在Hp感染的免疫应答中扮演着重要角色,参与胃炎、消化性溃疡、胃癌等Hp相关性疾病的发生发展。 Th17 cells are one of the CD4 ~ + T cell subtypes and can secrete inflammatory factors such as IL-17 and induce various diseases in the body. After Helicobacter pylori (Hp) infection, Cag A and Ure B can affect the number of Th17 cells, which may directly induce cell differentiation with infected macrophages and activate MyD88 signaling pathway and chemotactic factor The number of Th17 and Treg cells finally increased compared with that before infection, and the balance of Th17 / Treg was disturbed and shifted to the Treg in general. At the same time, increased Th17 cells could participate in the clearance of Hp by recruiting neutrophils and the like, on the other hand And expand the inflammatory response, causing mucosal damage or even induce canceration, and thus play an important role in the immune response of Hp infection, involved in the occurrence and development of Hp-related diseases such as gastritis, peptic ulcer, gastric cancer.