H. pylori infection induces persistent ICTM after eradication. Infection-driven iCAF differentiation contributes to epithelial malignant transformation and a potential immunosuppressive microenvironment, linking to gastric carcinogenesis. Our findings underscore the critical role of ICTM transformation, highlighting the need to improve ICTM for post-H. pylori eradication therapies, and indicate that specific iCAF subtypes represent promising intervention targets.
Fu et al. (Sun,) studied this question.