The T-lymphocyte is the primary cellular target for potentiation of the in vitro T-dependent IgM antibody response by the B subunit of cholera toxin

Abstract

The B (or binding) subunit of cholera toxin (CTB) was reported previously to potentiate the in vitro T-dependent IgM antibody response by a mechanism independent of the cyclic AMP-generating capacity of the intact toxin. In the present report, experiments were designed to determine the immune cell type mediating potentiation by CTB. Firstly, CTB did not potentiate T-independent antibody responses at concentrations that effectively enhanced T-dependent responses. Secondly, separation/reconstitution studies with splenocytes from CTB- and vehicle-treated mice demonstrated potentiation of T-dependent responses by CTB treatment of either the Sephadex G10 non-adherent population or the T-lymphocyte + macrophage population of cells. Potentiation was not observed by CTB treatment of the plastic adherent population or the B-lymphocyte + macrophage population. The evidence indicates that the T-lymphocyte is the primary cellular target for CTB-induced effects on the T-dependent IgM antibody response. Monosialoganglioside G M1, the putative binding site for CTB, is most likely the site of action for CTB on T-lymphocytes. These studies provide new insight on the mechanism of immunomodulation by cholera toxin, and CTB should provide a useful tool for further understanding the role of gangliosides in cellular immune responses.