Cimetidine, a H(2) receptor antagonist, has been reported to improve survival in
gastrointestinal cancer patients. These effects have largely been attributed to the enhancing effects of
cimetidine on the host's antitumour cell-mediated immune response, such as inhibition of suppressor T lymphocyte activity, stimulation of natural killer cell activity and increase of
interleukin-2 production from helper T lymphocytes. We conducted an in vitro study on the effects of
cimetidine on differentiation and
antigen presenting capacity of monocyte-derived dendritic cells from advanced
colorectal cancer patients and normal controls. As a result, an investigation of expression of surface molecules associated with dendritic cells by flow cytometric analyses showed that
cimetidine had no enhancing effect on differentiation of dendritic cells from
cancer patients and normal controls. An investigation of [(3)H]
thymidine incorporation by allogeneic mixed lymphocyte reactions revealed that
cimetidine increased the
antigen presenting capacity of dendritic cells from both materials. Moreover, a higher
antigen presenting capacity was observed in advanced
cancer patients compared to normal controls. These effects might be mediated via specific action of
cimetidine and not via H(2) receptors because
famotidine did not show similar effects. Our results suggest that
cimetidine may enhance the host's antitumour cell-mediated immunity by improving the suppressed dendritic cells function of advanced
cancer patients.