<italic>Helicobacter pylori </italic>Infection: Regulatory T Cells and Their Participation in the Immune Response

Abstract

A B S T R A C THelicobacter pylori (H. pylori) is a Gram-negative bacterium that colonizes the human stomach and affects more than half of the global human population. This microorganism shows variations in its geographical distribution and causes chronic gastritis, peptic ulcer, gastric adenocarcinoma and mucosa-associated lymphoid tissue lymphoma. The development of these clinical entities depends on the bacterial strain and its virulence, the host genetic predisposition, immunological response, concurrent infections and infestations.

The importance of Helicobacter pylori in the development of gastric MALT lymphoma — induction of proliferation and immune suppression

“…Elevated Treg cells level in the gastric mucosa is a key factor in reducing proliferation and cytotoxic activity of other T cells subpopulations, therapeutic failure and a poor prognosis [9,30,45,46]. Studies on Treg cell activity during an ongoing H. pylori infection may help to find new and effective therapies focused on oncogenesis control.…”

“…The course of tumor immunotherapy has shown that Treg-targeting compounds may be good candidates for treatment based on immune system modulation. Reducing Treg activity promotes the shift of the tumor microenvironment from being strongly suppressive to the physiologically active [45,46]. Among potential methods that can achieve this effect are: IL-10 receptor blockade [47], selectin blockade [48], inhibition of chemokines responsible for Treg cells recruitment (CCL17, CCL22, CCL20 or CXCL13), blocking chemokine receptors specifically expressed by Treg effector cells (e.g.…”

Role of Regulatory T Cells in the Helicobacter Pylori Infection

“…Investigations have implicated regulatory T cells (Tregs) in the pathogenesis of the H.pylori infection. Treg cells suppress excessive activation of CD4 + as well as CD8 + for controlling gastric inflammation and persistent colonization of the bacterium [1,2] . Studies have demonstrated that H.pylori-infected individuals have increased frequencies of CD4 + CD25 high T cells in both the stomach and duodenal mucosa compared to uninfected controls.…”

“…The inability of patients to clear H.pylori infections is a consequence of active immunosuppression and evasion mechanisms of bacteria. Many immune factors are involved: Dendritic cells (DCs) exhaustion by chronic exposure of these cells to H.pylori, influence of the immunosuppressive cytokines secreted by Tregs cells, mast cells that change the gastric mucosal environments among others [2] . Regulations of the Th17/Treg and Th1/Treg balances are important in the response immune in the H.pylori infection.…”

“…The identification of regulatory T cells and of their cytokines at the site of H.pylori infection in humans may also have important implications for the understanding of immune responses to other infections and also, the disruption of Treg function could contribute to the development of diverse autoimmune and inflammatory diseases. Nowadays, it is considered that the FOXp3 gen could be a therapeutic target to control of H.pylori infection take into consideration its participation in the development and function of Tregs cells [1,2] . …”