Helicobacter pylorirepresents a pathogen causing chronic infection in around a half of the global human population, which manifestations vary from asymptomatic infection to developing gastritis and peptic ulcer. The data accumulated suggest that overt clinical types of this infection are associated with lost immunoregulation and increased pro-inflammatory cell-mediated immune response triggered byH. pylori-specific T helper cells. Here, we examined the degree of peripheral blood CD4+T cell maturity and related expression of chemokine receptors involved in migration to gastrointestinal tract (CCR9 and CCR6), as well as Тand B-cell zones of lymphoid organs (CCR7 and CXCR5). It was shown that overtH. pylori-infection was coupled to changes in expression pattern of chemokine receptors on T helper cells. In particular, percentage of mature CD4+CD45RO+T cells bearing CCR9 and immature CD4+CD45RO–Т cells expressing CXCR5 was increased in peripheral blood of patients with chronic gastroduodenitis. However, increased amount of activated mature CD4+CD45RO+ICOS+T cells was observed in patients with chronic gastroduodenitis comorbid with peptic ulcer that was also associated with elevated amount of mature CCR6+T helpers (mainly CD4+CD45RO+CCR7–CCR6+cells) and follicular T helper cells as well as emerging minor CD4+CD45RO+CXCR5+CCR6+.T cell subset, not affecting CD4+CCR9+Т cells. Thus, the data obtained evidence that tissue-specific T-helper cell migration is controlled separately in ofH. pylori-associated diseases.
Unveiling the Intricacies of Helicobacter pylori-Induced Gastric Inflammation: T Helper Cells and Matrix Metalloproteinases at a Crossroad