CagA-specific Gastric CD8+ Tissue-Resident T Cells Control Helicobacter pylori During the Early Infection Phase

Helicobacter pylori induces urease subunit B‐specific CD8+ T cell responses in infected individuals via cytosolic pathway of cross‐presentation

“…Previously, we also found that the frequency of CD8 + T cells in the gastric tissue of patients with H. pylori infection was higher than that of healthy participants 39 . Our observations are consistent with the study of Koch 14 that infection with H. pylori initially induces a strong infiltration of gastric CD8 + T cells in infected patients and mice. Given that human gastric tissue was difficult to obtain clinically and gastric primed T cells were recruited from peripheral circulation to mucosal tissues, peripheral blood samples from H. pylori‐ infected individuals were used to induce the expansion of H. pylori ‐specific CD8 + T cells.…”

“…However, the host CD4 + T cell immune response could not prevent the chronic persistent infection by H. pylori . Recent studies had focused on CD8 + T cell immune response and suggested that specific CD8 + T cells infiltrating the gastric mucosa participated in the response to H. pylori 13–16 . H. pylori derived antigen specific CD8 + T cells have not been clearly identified and the mechanisms underlying the production of the specific CD8 + T cell responses deserve to be explored in depth.…”

“…Actually, the immune role of specific CD8 + T cell responses in H. pylori infection remains controversial. A study of Koch 14 demonstrated that infection with H. pylori initially induces a strong infiltration of protective gastric CD8 + T cells in infected patients and mice. Ratnasari 50 reported a negative correlation between gastric lesions with CD8 + T cells infiltration in H. pylori infected subjects, indicating CD8 + T cells play a protective role in host immunity.…”

“…Previous studies have confirmed the effectiveness of UreB in generating CD4 + T cell‐mediated protection, 12 but less is known regarding CD8 + T cell immune response to H. pylori UreB. Recent studies had focused on CD8 + T cell immune response and suggested that specific CD8 + T cells infiltrating the gastric mucosa participated in the resistance to H. pylori infection in mice, but its functions were still controversial 13–16 …”

Tissue-resident memory T cells in gastrointestinal tumors: turning immune desert into immune oasis

“…A recent study has shown that CagA-specific CD8 + Trm cells can infiltrate the gastric mucosa and control the H. pylori. infection ( 98 ). EBV infection can induce DNA demethylation of host cells, which results in expression of tumor suppressor genes, loss of tumor-related antigens, and over-expression of immune checkpoint like PD-L1 and PD-L2 and induces immune evade of Epstein–Barr virus-associated gastric cancer (EBVaGC) by PD-1/PD-L1 interactions between tumor cells and T cells ( 99 , 100 ).…”