부산대학교 도서관

ABSTRACTPersistent colonization of the human stomach by Helicobacter pyloriis a risk factor for the development of gastric cancer and peptic ulcer disease. H. pylorisecretes a toxin, VacA, that targets human gastric epithelial cells and T lymphocytes and enhances the ability of H. pylorito colonize the stomach in a mouse model. To examine how VacA contributes to H. pyloricolonization of the mouse stomach, we investigated whether murine T lymphocytes were susceptible to VacA activity. VacA inhibited interleukin-2 (IL-2) production by a murine T-cell line (LBRM-33), similar to its effects on a human T-cell line (Jurkat), but did not inhibit IL-2 production by primary murine splenocytes or CD4+T cells. VacA inhibited activation-induced proliferation of primary human CD4+T cells but did not inhibit the proliferation of primary murine CD4+T cells. Flow cytometry studies indicated that the levels of VacA binding to primary murine CD4+T cells were significantly lower than levels of VacA binding to human CD4+T cells. This suggests that the resistance of primary murine CD4+T cells to VacA is attributable, at least in part, to impaired VacA binding to these cells.