In order to characterize T cell responses in human Helicobacter pylori infe
ction, we have examined proliferative responses and cytokine production by
CD4(+) and CD8(+) T cells isolated from duodenal ulcer patients and asympto
matic H. pylori carriers, after activation with some H. pylori antigens tha
t may be important in disease development. For control purposes, T cells fr
om uninfected volunteers were also examined. The different H. pylori antige
ns induced only modest proliferative responses in circulating CD4(+) and CD
8(+) T cells from both H. pylori-infected and uninfected individuals. Howev
er, circulating T cells from H. pylori-infected subjects produced larger am
ounts of interferon-gamma (IFN-gamma) in response to the Helicobacter antig
ens than did T cells from uninfected volunteers. Furthermore, CD8(+) T cell
s produced larger amounts of IFN-gamma than did CD4(+) T cells, on a per ce
ll basis. Most IFN-gamma -producing cells from both infected and uninfected
volunteers appeared to be naive T cells expressing CD45RA. Increased produ
ction of IL-4 and IL-5 was, on the other hand, only seen in a few instances
after stimulation of isolated CD4(+) and CD8(+) T cells. Stimulation of fr
eshly isolated gastric T cells with the different H. pylori antigens did no
t result in increased proliferation or cytokine production. In conclusion,
our results show that several different purified H. pylori antigens induce
production of IFN-gamma, preferentially by CD8(+) cells. Therefore, they su
ggest that IFN-gamma -secreting CD8(+) cells contribute significantly to th
e cytokine response induced by H. pylori infection.