Immune Responses Mediated by Th17 Cells in Helicobacter pylori Infection

T helper 17 (Th17) cells are one of the CD4+ T-cell subsets which induce a variety of diseases by secreting IL-17 and other inflammatory factors. After Helicobacter pylori (Hp) infection, cytotoxin-associated gene A and urease subunit B regulate the number of Th17 cells via induction of cell differentiation by infected macrophages, activation of MyD88 and other pathways, and by driving chemokines, which upregulates the number of both Th17 cells and regulatory T cells (Tregs) and switches towards a Treg-type immune response. Meanwhile, Th17 cells also play important roles in the response to Hp infection, participating in the clearance of Hp by recruiting neutrophils and expanding inflammatory response, causing mucosal damage and even inducing cancer. Thereby, Th17 cells participate in the occurrence and development of Hp-related diseases, such as gastritis, peptic ulcer disease and gastric cancer.