白介素-17及其相关信号通路支持幽门螺杆菌诱导胃癌发生的机制研究进展  

IL-17 and Its Signaling Pathways Mediate Helicobacter Pylori Inducing Gastric Cancer

作　　者：陈雨甜 徐红[1] 陈红玲 陈洁[1] CHEN Yutian;XU Hong;CHEN Hongling;CHEN Jie(First Affiliated Hospital of Soochow University,Suzhou 215000,China)

机构地区：[1]苏州大学附属第一医院,江苏苏州215000

出　　处：《肿瘤学杂志》2023年第10期840-846,共7页Journal of Chinese Oncology

摘　　要：幽门螺杆菌感染作为胃癌的Ⅰ类致癌原,其引起的慢性炎症-萎缩性胃炎-萎缩性胃炎伴肠上皮化生-异型增生而逐渐向胃癌演变,而IL-17作为关键的促炎细胞因子之一,IL17+细胞和相关信号通路参与胃癌的发生、进展,并与胃癌预后不良相关。全文综述IL-17介导胃癌发生、进展、治疗耐药、转移的可能机制,包括促进细胞增殖、抑制细胞凋亡,创造免疫耐受微环境,诱导T细胞耗竭,持续的血管生成,以及诱导上皮-间充质转化。Helicobacter pylori infection,as a class I carcinogen of gastric cancer,causes chronic inflammation evolving to atrophic gastritis,intestinal metaplasia,dysplasia,and eventually to gastric cancer.IL-17,as one of the key pro-inflammatory cytokines,is involved in the occurrence and development of gastric cancer;and IL-17+cells and related signaling pathways are closely associated with poor prognosis of gastric cancer.This paper reviews the possible mechanisms by which IL-17 mediates the development,metastasis and treatment resistance of gastric cancer,in-cluding promoting cell proliferation,inhibiting cell apoptosis,creating an immune-tolerant mi-croenvironment,causing T cell exhaustion,sustaining angiogenesis,and inducing epithelial-mes-enchymal transition.

关 键 词：胃肿瘤 白介素-17 幽门螺杆菌 肿瘤免疫微环境 髓源性抑制细胞 T细胞耗竭 

分 类 号：R735.2[医药卫生—肿瘤]