Il-2 receptor expression on gastric mucosa T lymphocytes is enhanced in duodenal ulcer patients compared with non-ulcer dyspeptic patients.
Аннотация
BACKGROUND/AIMS: Helicobacter pylori infects an estimated 50% of the world population, however only a small proportion of individuals develop clinical symptoms of gastritis, peptic ulceration or gastric cancer. The variations in disease presentation may be due to differences in bacterial virulence and/or immune response to the pathogen. This study examined the expression of IL-2 receptor and ICAM-1 molecules on gastric mucosa infiltrating T lymphocytes in two groups of H. pylori infected patients: one group with an active ulcer disease and the other with non-ulcerative chronic gastritis.
MATERIAL AND
METHODS
T lymphocytes were isolated from gastric mucosa biopsies by using mechanical and enzymatic tissue desegregation. Ficoll-purified lymphocytes were incubated with monoclonal antibodies and analyzed by using 3-color flow cytometry analysis for the IL-2 receptor (CD25) and ICAM-1 molecule (CD54) expression. Lymphocytes from 37 Helicobacter pylori infected patients with severe gastric mucosa infiltration (G2 and G3 histological type in Sydney classification) were analyzed; 18 patients had at least 5-year history of duodenal ulcer disease (group A) and 19 patients had at least 3-year history of non-ulcer dyspeptic disease (group B).
RESULTS
We demonstrated a significant increase in IL-2 receptor expression on gastric mucosa T cells in ulcer patients (group A) compared with non-ulcer dyspeptic patients (group B). However, no difference in CD54 expression was found between the two groups of patients.
CONCLUSIONS
Our results suggest the importance of the local immune response in the development of H. pylori related diseases. Also some interesting points for further study of the association between immune response against H. pylori and the development of duodenal ulcer disease were indicated.
Предметные рубрики MeSH
Подготовка и перевод публикации
Обработка статьи · этапы, ошибки и управление
Ошибки и ограничения
История · было → стало
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