A. Ihan et al., IL-2 RECEPTOR EXPRESSION ON GASTRIC-MUCOSA T-LYMPHOCYTES IS ENHANCED IN DUODENAL-ULCER PATIENTS COMPARED WITH NONULCER DYSPEPTIC PATIENTS, Hepato-gastroenterology, 43(12), 1996, pp. 1665-1670
Background/Aims: Helicobacter pylori infects an estimated 50% of the w
orld population, however only a small proportion of individuals develo
p 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. gas
tric mucosa infiltrating T lymphocytes in two groups of H. pylori infe
cted patients: one group with an active ulcer disease and the other wi
th non-ulcerative chronic gastritis. Material and Methods: T lymphocyt
es were isolated from gastric mucosa biopsies by using mechanical and
enzymatic tissue desegregation. Ficoll-purified lymphocytes were incub
ated with monoclonal antibodies and analyzed by using S-color flow cyt
ometry analysis for the IL-2 receptor (CD25) and ICAM-1 molecule (CD54
) expression. Lymphocytes from 37 Helicobacter pylori infected patient
s 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 a
t Least 3-year history of non-ulcer dyspeptic disease (group B). Resul
ts: 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 true groups of patients. Conclusions
: Our results suggest the importance of the local immune response in t
he development of H. pylori related diseases. Also some interesting po
ints for further study of the association between immune response agai
nst H. pylori and the development of duodenal Jeer disease were indica
ted.