Anti-IgM-Ficoll conjugates activate B cells from CBA but not CBA/N mice.

We have compared the stimulating effects of an anti-IgM-Ficoll conjugate on B cells from the two mouse strains CBA and CBA/N. CBA/N mice have a recessive defect on their X chromosome which make them unable to respond to T1-2 antigens and B cells from these mice are supposed to be in an immature state. We found that the anti-IgM-Ficoll conjugate stimulated B cells of the CBA strain to proliferate even without the addition of interleukins, but was not able to stimulate B cells from the CBA/N strain. To rule out that the unresponsiveness of CBA/N mice to anti-IgM-Ficoll was due to the immaturity of their B cells, we cultured B cells from both strains in the presence of an anti-IgM-Sepharose conjugate. This conjugate stimulated B cells from both mouse strains to proliferate in the presence of IL-4. These results agree with the hypothesis that the T1-2 antigen Ficoll is able to deliver activating signals to B cells and therefore cannot be considered as an inert carrier.