Captopril and immune regulation.
We examined the in vitro effect of captopril (2.5 to 5 micrograms/ml) on the primary antibody response of human B cells. Captopril suppresses (by 50%) the specific anti-trinitrophenyl (TNP) response of unfractionated peripheral blood mononuclear cells (PBM) but not that of nonadherent PBM. The susceptibility to captopril suppression can be restored in the latter cell cultures by 10% adherent radioresistant cells. This suppression is independent of prostaglandins. In transfer experiments, cells preincubated with 5 micrograms/ml captopril suppress the antibody response of autologous nonadherent PBM. The inductive phase of this suppression requires both adherent cells and radiosensitive T cells. Once induced, the suppression can be transferred by isolated T effector cells. In vivo after a unique oral intake of captopril a moderate suppressor activity can be demonstrated in adherent cells from normal individuals. We conclude that captopril interferes with the immune regulation by inducing a suppressor circuit involving monocytes and a T8 suppressor effector lymphocyte.
D000917:Antibody Formation / Q000187:drug effects*; D001402:B-Lymphocytes / Q000187:drug effects*; D002216:Captopril / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D006801:Humans; D007213:Indomethacin / Q000494:pharmacology; D009000:Monocytes / Q000187:drug effects; D011392:Proline / Q000031:analogs & derivatives*; D013601:T-Lymphocytes / Q000187:drug effects*; D050378:T-Lymphocytes, Regulatory / Q000187:drug effects
D011392:Proline; D002216:Captopril; D007213:Indomethacin