Mucosal FOXP3-expressing CD4+ CD25high regulatory T cells in Helicobacter pylori-infected patients

Anna Lundgren, Erika Strömberg, Åsa Sjöling, Catharina Lindholm, Karin Enarsson, Anders Edebo, Erik Johnsson, Elisabeth Suri-Payer, Pia Larsson, Anna Rudin, Ann Mari Svennerholm, B. Samuel Lundin

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231 Citations (Scopus)


Helicobacter pylori chronically colonizes the stomach and duodenum and causes peptic ulcers or gastric adenocarcinoma in 10 to 20% of infected individuals. We hypothesize that the inability of patients to clear H. pylori infections is a consequence of active suppression of the immune response. Here we show that H. pylori-infected individuals have increased frequencies of CD4+ CD25high T cells in both the stomach and duodenal mucosa compared to uninfected controls. These cells have the phenotype of regulatory T cells, as they express FOXP3, a key gene for the development and function of regulatory T cells, as well as high levels of the cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) protein. In contrast, mucosal CD4 + CD25low and CD4+ CD25- cells express little FOXP3 mRNA and low levels of the CTLA-4 protein. Mucosal CD4 + CD25high T cells are present in individuals with asymptomatic H. pylori infections as well as in duodenal ulcer patients. The frequencies of CD4+ CD25high cells are also increased in the stomachs of A pylori-infected patients with gastric adenocarcinoma, particularly in cancer-affected tissues. These findings suggest that regulatory T cells may suppress mucosal immune responses and thereby contribute to the persistence of H. pylori infections.

Original languageEnglish
Pages (from-to)523-531
Number of pages9
JournalInfection and Immunity
Issue number1
Publication statusPublished - 1 Jan 2005
Externally publishedYes

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