Function and recruitment of mucosal regulatory T cells in human chronic Helicobacter pylori infection and gastric adenocarcinoma

2006 ◽  
Vol 121 (3) ◽  
pp. 358-368 ◽  
Author(s):  
Karin Enarsson ◽  
Anna Lundgren ◽  
Bert Kindlund ◽  
Mikael Hermansson ◽  
Giovanna Roncador ◽  
...  
2005 ◽  
Vol 73 (1) ◽  
pp. 523-531 ◽  
Author(s):  
Anna Lundgren ◽  
Erika Strömberg ◽  
Åsa Sjöling ◽  
Catharina Lindholm ◽  
Karin Enarsson ◽  
...  

ABSTRACT 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 H. 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.


2011 ◽  
Vol 121 (8) ◽  
pp. 3088-3093 ◽  
Author(s):  
Isabelle C. Arnold ◽  
Nina Dehzad ◽  
Sebastian Reuter ◽  
Helen Martin ◽  
Burkhard Becher ◽  
...  

2016 ◽  
Vol 47 (4) ◽  
pp. 245-254 ◽  
Author(s):  
Nader Bagheri ◽  
Fatemeh Azadegan-Dehkordi ◽  
Ghorbanali Rahimian ◽  
Mahmoud Rafieian-Kopaei ◽  
Hedayatollah Shirzad

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