Conventional, Regulatory, and Unconventional T Cells in the Immunologic Response to Helicobacter pylori

Abstract

Infection by the gastroduodenal pathogen Helicobacter pylori elicits a complex immunologic response in the mucosa involving neutrophils, plasma cells, eosinophils, and lymphocytes, of which T cells are the principal orchestrators of immunity. While so-called classical T cells (e.g. T-helper cells) that are activated by peptide fragments presented on antigen-presenting cells have received much attention in H. pylori infection, there exists a diverse array of other T cell populations that are potentially important for the outcome of the ensuing immune response, some of which have not been extensively studied in H. pylori infection. Pathogen-specific regulatory T cells that control and prevent the development of immunopathology associated with H. pylori infection have been investigated, but these cells can also benefit the bacterium in helping to prolong the chronicity of the infection by suppressing protective immune responses. An overlooked T cell population, the more recently described Th17 cells, may play a role in H. pylori-induced inflammation, due to triggering responses that ultimately lead to the recruitment of polymorphs, including neutrophils. The so-called innate or unconventional T cells, that include two conserved T cell subsets expressing invariant antigen-specific receptors, the CD1d-restricted natural killer T cells which are activated by glycolipids, and the mucosal-associated invariant T cells which play a role in defense against orally acquired pathogens in the intestinal mucosa, have only begun to receive attention. A greater knowledge of the range of T cell responses induced by H. pylori is required for a deeper understanding of the pathogenesis of this bacterium and its ability to perpetuate chronic infection, and could reveal new strategies for therapeutic exploitation.

Helicobacter pylori Promotes the Production of Thymic Stromal Lymphopoietin by Gastric Epithelial Cells and Induces Dendritic Cell-Mediated Inflammatory Th2 Responses

“…In this study, we demonstrated that H. pylori triggered human gastric epithelial cells to produce TSLP, together with MIP-3␣ and BAFF. Because H. pylori products induce NF-B activation in gastric epithelial cells (8,27,41,47), H. pylori-induced NF-B activation in gastric epithelial cells may directly and/or indirectly upregulate the expression of TSLP, MIP-3␣, and BAFF in these cells.…”

Helicobacter pylori as a trigger and aggravating factor in rheumatoid arthritis and other rheumatic diseases

“…Хотя H. pylori индуцирует гуморальный и клеточный иммунный ответ, он несовершенен и не позволяет элими-нировать этот микроорганизм [35]. Факторы вирулентности бактерии, такие как Vac A (vacuolating cytotoxin A), островок патогенности (cag PAI), белок теплового шока (heat shock protein, HSP 60), способны ингибировать Т-клеточную про-лиферацию и нарушать созревание дендритных клеток [36].…”

Animal Models of H. pylori Infection

“…In contrast, the B-cell-defi cient μMT mice infected with H. felis exhibited severe pathological changes in the stomach such as mucosal hyperplasia and intestinal metaplasia, which was similar to the normalstate immune responses of C57BL/6 mice [ 27 ]. T cells plays the most important role in the immune responses to H. pylori infection [ 28 ], and the balance of Th1/Th2 immune responses are essential in the pathogenesis of H. pylori -associated disease and host defense mechanisms (Fig. 55.1 ).…”