Intraperitoneal administration of the B subunit of Escherichia coli enterotoxin to mice temporarily decreased the numbers of CD5⁺CD45⁺ double-positive cells, CD5⁺ B cells, in peritoneal cavity. In vitro, CD5⁺ B cells treated with the B subunit decreased in number like in vivo but did not recover. Functionally, the peritoneal cells stimulated by the B subunit in vitro produced immunoglobulin M (IgM) in a dose- and time-dependent manner. A mutant defective in binding to GM1-ganglioside significantly reduced less number of CD5⁺ B cell and did not increase production of IgM than the B subunit. Although the apoptosis in CD5⁺ B cell fraction was not detected, a new fraction containing CD5^-CD45^- double-negative cells appeared in vitro following by reduction of CD5⁺ B cells and partially underwent apoptosis.

These results suggest that the B subunit reduces the number of CD5⁺ B cells and stimulates production of IgM dependent on its binding to GM1-ganglioside. CD5⁺ B cells stimulated by the B subunit might lose their specific antigens to produce IgM and after die with apoptosis.