TY - JOUR
T1 - Mucosal FOXP3-expressing CD4+ CD25high regulatory T cells in Helicobacter pylori-infected patients
AU - Lundgren, Anna
AU - Strömberg, Erika
AU - Sjöling, Åsa
AU - Lindholm, Catharina
AU - Enarsson, Karin
AU - Edebo, Anders
AU - Johnsson, Erik
AU - Suri-Payer, Elisabeth
AU - Larsson, Pia
AU - Rudin, Anna
AU - Svennerholm, Ann Mari
AU - Lundin, B. Samuel
PY - 2005/1/1
Y1 - 2005/1/1
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=19944404220&partnerID=8YFLogxK
U2 - 10.1128/IAI.73.1.523-531.2005
DO - 10.1128/IAI.73.1.523-531.2005
M3 - Article
C2 - 15618192
AN - SCOPUS:19944404220
VL - 73
SP - 523
EP - 531
JO - Infection and Immunity
JF - Infection and Immunity
SN - 1098-5522
IS - 1
ER -