Like most solid tumours, the microenvironment of epithelial-derived gastric adenocarcinoma (GAC) consists of a variety of stromal cell types, including fibroblasts, and neuronal, endothelial and immune cells. In this article, we review the role of the immune microenvironment in the progression of chronic inflammation to GAC, primarily the immune microenvironment driven by the gram-negative bacterial species Helicobacter pylori. The infection-driven nature of most GACs has renewed awareness of the immune microenvironment and its effect on tumour development and progression. About 75–90% of GACs are associated with prior H. pylori infection and 5–10% with Epstein–Barr virus infection. Although 50% of the world’s population is infected with H. pylori, only 1–3% will progress to GAC, with progression the result of a combination of the H. pylori strain, host susceptibility and composition of the chronic inflammatory response. Other environmental risk factors include exposure to a high-salt diet and nitrates. Genetically, chromosome instability occurs in ~50% of GACs and 21% of GACs are microsatellite instability-high tumours. Here, we review the timeline and pathogenesis of the events triggered by H. pylori that can create an immunosuppressive microenvironment by modulating the host’s innate and adaptive immune responses, and subsequently favour GAC development.

与大多数实体瘤一样，上皮源性胃腺癌 (GAC) 的微环境由多种基质细胞类型组成，包括成纤维细胞、神经元细胞、内皮细胞和免疫细胞。在这篇文章中，我们回顾了免疫微环境在慢性炎症发展为 GAC 中的作用，主要是革兰氏阴性菌幽门螺杆菌驱动的免疫微环境。大多数 GAC 的感染驱动特性重新认识了免疫微环境及其对肿瘤发展和进展的影响。大约 75-90% 的 GAC 与既往幽门螺杆菌感染有关，5-10% 与 EB 病毒感染有关。虽然世界上50%的人口感染了幽门螺杆菌, 只有 1-3% 会进展为 GAC，进展是幽门螺杆菌菌株、宿主易感性和慢性炎症反应的组合的结果。其他环境风险因素包括接触高盐饮食和硝酸盐。在遗传学上，染色体不稳定性发生在约 50% 的 GAC 中，而 21% 的 GAC 是微卫星不稳定性高的肿瘤。在这里，我们回顾了幽门螺杆菌引发的事件的时间表和发病机制，这些事件可以通过调节宿主的先天性和适应性免疫反应来创造免疫抑制微环境，并随后有利于 GAC 的发展。