Gastric cancer is one of the leading causes of cancer deaths worldwide, with chronic gastritis representing the main predisposing factor initiating the cascade of events leading to metaplasia and eventually progressing to cancer. A widely accepted classification distinguishes between autoimmune and environmental atrophic gastritis, mediated, respectively, by T cells promoting the destruction of the oxyntic mucosa, and chronicH. pyloriinfection, which has also been identified as the major risk factor for gastric cancer. The original dogma posits Th1 immunity as a main causal factor for developing gastritis and metaplasia. Recently, however, it has become evident that Th2 immune responses play a major role in the events causing chronic inflammation leading to tumorigenesis, and in this context, many different cell types and cytokines are involved. In particular, the activity of cytokines, such as IL-33 and IL-13, and cell types, such as mast cells, M2 macrophages and eosinophils, are intertwined in the process, promoting chronic gastritis-dependent and more diffuse metaplasia. Herein, we provide an overview of the critical events driving the pathology of this disease, focusing on the most recent findings regarding the importance of Th2 immunity in gastritis and gastric metaplasia.
胃癌是全球癌症死亡的主要原因之一，慢性胃炎是启动从化生到最终癌变级联反应的主要诱发因素。目前广泛接受的分类方法将萎缩性胃炎分为自身免疫性和环境性两类，前者由T细胞介导的泌酸黏膜破坏引发，后者则由幽门螺杆菌慢性感染导致——该病原体已被确定为胃癌的主要风险因素。传统理论认为Th1免疫反应是胃炎和化生发展的主要致病因素。然而近年研究表明，Th2免疫应答在导致慢性炎症及最终肿瘤发生的过程中发挥着关键作用，这一过程涉及多种细胞类型和细胞因子的参与。特别是IL-33、IL-13等细胞因子以及肥大细胞、M2型巨噬细胞和嗜酸性粒细胞等细胞类型，在该过程中相互交织作用，促进慢性胃炎依赖性及更广泛分布的化生发生。本文系统阐述了驱动该疾病病理发展的关键环节，重点关注Th2免疫在胃炎和胃化生中重要作用的最新研究进展。
肿瘤(癌症)患者之家