Vaccine‐induced gastric CD4 + tissue‐resident memory T cells proliferate in situ to amplify immune response against Helicobacter pylori insult

Background Tissue‐resident memory T cells accelerate the clearance of pathogens during recall response. However, whether CD4 + TRM cells themselves can provide gastric immunity is unclear. Materials and methods We established a parabiosis model between the enhanced green fluorescent protein and wild‐type mice that the circulation system was shared, and the wild‐type partner was vaccinated with H pylori vaccine composed of CCF and silk fibroin in gastric subserous layer to induce gastric EGFP + CD4 + TRM cells. Antigen‐specific EGFP + CD4 + T cells and proliferous TRM cells were analyzed by flow cytometry. The colonization of H pylori was detected by quantitative real‐time PCR. EGFP + CD4 + TRM cells and the inflammation of the stomach were observed by histology. Results A parabiosis animal model was employed to identify the cells that introduced by vaccination in GSL. Antigen‐specific EGFP + CD4 + T cells could be detected at day 7 post‐vaccination. Thirty days later, EGFP + CD4 + TRM cells were established with a phenotype of CD69 + CD103 ‐ . Of note, we found that when circulating lymphocytes were depleted by FTY720 administration, these TRM cells could proliferate in situ and differentiate into effector Th1 cells after H pylori challenge. A decrease in H pylori colonization was observed in the vaccinated mice but not unvaccinated mice. Further, we found that although FTY720 was administrated, mounted pro‐inflammatory myeloid cells still emerged in the stomach of the vaccinated mice, which might contribute to the reduction of H pylori colonization. Conclusions Our study reveals that H pylori vaccine‐induced CD4 + TRM cells can proliferate and differentiate in situ to enhance gastric local immunity during recall response.