Abstract
Colchicine (CC) enhances the antibody response in mice to protein antigens, like diphtheria toxoid and human .gamma.-globulin, and to the trinitrophenyl hapten. Maximal enhancement was observed when CC was administered to animals on the same day as the injection of antigen. The optimal dose of CC was in the range of 1.0-1.5 mg/kg body weight. The enhanced antibody formation was evident from elevated circulating antibody titers and from an increased number of antibody plaque-forming cells (PFC) of the spleen. The circulating antibody titer of CC-treated animals was higher than that of control animals by a factor of about 3-7 in the primary response, and by a factor of at least 15 in the secondary response. In terms of the number of antibody forming ells, CC enhanced the primary PFC response by .simeq. 100%, and the secondary PFC response by as high as 5-fold. The enhancing effect of CC seemed to be related to its mitosis-blocking capacity since vinblastine, another antimototic drug, was as effective as CC and lumicolchicine, the non-anti-mitotic structural isomer of CC, was ineffective in potentiating antibody responses. The critical timing in the administration of CC on the same day as antigen suggests that most likely, the mitotic poison was acting on antigen-stimulated early dividing suppressor cells.