Helicobacter pylori and mucosa-associated lymphoid tissue: what's new

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

“…Lymphoid tissue is physiologically absent from the stomach. However, due to chronic H. pylori infection and an infiltration of immune cells, gastric MALT lymphomas can arise [9]. MALT lymphoma cells share the same cytological and immunophenotypical features: i.e.…”

“…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.…”

“…Treg cells recruitment occurs through secretion of CCL17 and CCL22 chemokines produced by B cells [32]. Treg cells promote tolerogenic signals and secrete anti-inflammatory cytokines, such as IL-10 and TGF-b [9,30]. IL-10 increases the B cells ability to proliferate, survive and differentiate.…”

“…This process is characteristic of the initial stages of H. pylori infection. The next step is based on the host immune response being suppressed by over-activation of CD4 + CD25 + (Treg cells) [9,30,31]. Treg cells recruitment occurs through secretion of CCL17 and CCL22 chemokines produced by B cells [32].…”

“…large B-cell lymphoma (DLBCL), systemic polychemotherapy is recommended for first-line treatment despite the coexisting H. pylori infection. Patients therapy whenever advanced-stage disease occurs and in those with confirmed lymphoma recurrence is based on chlorambucil, fludarabine and rituximab treatment [5,7,9,41].…”