The roles of tissue resident T cells during H. pylori infection and after immunization

Helicobacter pylori infection is one of the most common bacterial infection worldwide. Gastric colonization with H. pylori can lead to various upper gastrointestinal disorders, such as gastritis, peptic ulcer disease, gastric mucosa-associated lymphoid tissue (MALT) lymphoma, and gastric cancer. Different immune cell subsets can be found in the stomach of infected subjects. In particular, T cells have been shown to infiltrate and highly contribute to gastric inflammation in order to control the infection. Tissue-resident memory T cells (T_RM) have been recently described as important players in the immune response against different infections. They reside in the non-lymphoid tissues without entering recirculation, and after most infections they emerge after the resolution of local inflammation. Therefore, they can rapidly react to local infection by forming secondary T_RM cells from pre-existing T_RM cells or from their precursors recruited from the circulation. Effector T cells within non-inflamed tissues can also differentiate into T_RM cells after adaption to local chemokines. T_RM cells are present during H. pylori infection. However, their putative functions have not been clearly defined. Moreover, the contribution of H. pylori virulence factors to the induction of T_RM cells remains unclear. Therefore, we explore the function of stomach T_RM cells after H. pylori infection, and the contribution of different H. pylori virulence factors to the induction of T_RM cell responses. Further, we want to analyse the relevance of T_RM cells for protection upon prophylactic immunization (see ● Vaccine development against H. pylori).