Abstract
In general, breeding pairs are not major histocompatibility complex (MHC)-compatible, and therefore the fetoplacental unit can be considered as a natural allograft. In many mammals pregnancy leads to the production of nonlytic antibodies of antipaternal MHC specificity. It has been suggested that these protect the semiallogeneic fetus from rejection by acting as blocking or enhancing factors-or, alternatively, that they are part of a humoral response involved in the establishment of a humoral response involved in the establishment of normal pregnancy. These hypotheses were tested in allomated mice made B cell deficient by continuous treatment with .alpha.IgM.mu. antiserum. The status of the maternal immune system was assessed by in vivo antibody production, in vitro mitogen responses, and allograft rejection. By these criteria B cell function could not be demonstrated in .alpha.IgM.mu. treated female mice, but T cell responses were unaffected. Allogeneic pregnancy, however, was not compromised by this humoral immune system dysfunction-litter size and neonatal survival being the same in the .alpha.IgM.mu. and control serum-treated groups. These results indicate that a maternal humoral immune response is not essential for the establishment of pregnancy or the survival of the semiallogeneic fetus.