Pregnancy in B-cell-deficient mice: postpartum transfer of immunoglobulins prevents neonatal runting and death.

Mice lacking functional B cells because of a genetic deletion of the mu chain (IgM) gene were used to investigate the role of perinatal and postnatal transfer of maternal IgG in neonatal growth. Our results confirmed that immunoglobulin (Ig)-deficient mice successfully complete pregnancy and deliver healthy offspring. However, neonates nursed by Ig-deficient mothers showed growth retardation (runting) and high mortality during their first 10 days of life. This fatal course was seen whether or not the neonates were Ig-deficient. Cross-switching litters from phenotypically normal mothers to Ig-deficient mothers immediately after birth showed that perinatal Ig transfer normalized neonatal development for 10 days, but was not sufficient to sustain survival during the later part of the neonatal period. On the other hand, all Ig-deficient litters nursed by normal foster mothers showed normal development and 0% neonatal mortality. Administration of mouse IgG to an Ig-deficient mother or a neonate during the first critical week prevented runting. We assume that the growth- and health-promoting effects of IgG during early neonatal life are attributable mainly to the transfer of passive immunity to environmental pathogens. However, the finding that monoclonal IgG antibodies also enhanced neonatal growth and survival suggests that IgG-dependent growth-promoting mechanisms could be involved as well.