LYMPHOCYTES IN THE HUMAN GASTRIC-MUCOSA DURING HELICOBACTER-PYLORI HAVE A T-HELPER CELL-1 PHENOTYPE

Citation
Kb. Bamford et al., LYMPHOCYTES IN THE HUMAN GASTRIC-MUCOSA DURING HELICOBACTER-PYLORI HAVE A T-HELPER CELL-1 PHENOTYPE, Gastroenterology, 114(3), 1998, pp. 482-492
Citations number
48
Categorie Soggetti
Gastroenterology & Hepatology
Journal title
ISSN journal
00165085
Volume
114
Issue
3
Year of publication
1998
Pages
482 - 492
Database
ISI
SICI code
0016-5085(1998)114:3<482:LITHGD>2.0.ZU;2-S
Abstract
Background & Aims: Studies have shown that gastric T cells are increas ed during Helicobacter pylori infection. The purpose of this study was to characterize the human gastric T-cell responses in the presence or absence of H. pylori. Methods: T-cell surface antigens were examined by immunohistochemistry or after isolation for evaluation of surface a ntigens and cytoplasmic cytokines using flow cytometry. Results: CD4() and CD8(+) T cells were increased in situ during infection with H. p ylori. Freshly isolated gastric T cells expressed cytoplasmic interfer on gamma (IFN-gamma) and interleukin (IL)-2 after a brief stimulation. Simultaneous four-color flow cytometry demonstrated that both CD8(+) and CD4(+) T cells expressed IFN-gamma. Because stimulation through CD 30 favors the induction of IL-5 and Th2 cells, gastric and colonic T c ells were examined for CD30 expression. Consistent with the notion tha t Th2 cells are found in the intestine, CD30 was evident throughout th e lamina propria of the colon but was virtually absent in the stomach. Furthermore, freshly isolated gastric T cells produced little IL-4 an d virtually no IL-5 or tumor necrosis factor beta. Conclusions: These observations show that gastric T cells resemble the Th1 type, which ma y explain their failure to induce immunity to H. pylori and their abil ity to contribute to the pathogenesis of gastric disease.