Maternal immunity protects offspring from enteric viral infection without negatively affecting humoral immune memory

Passive transfer of antibodies can effectively protect newborns from dysbiosis and infection but has also been proposed to inhibit intrinsic immune onset in the protected child. Yet, some early childhood vaccines are highly efficacious despite the presence of maternal antibodies. We here used a murine neonatal Rotavirus (RV) infection model in combination with cross-foster approaches to dissect the role that milk-derived antibodies play in the long-term induction of pup-intrinsic immunity. We found that milk-derived RV-specific antibodies efficiently protect from RV infection. While the occurrence of RV-specific IgA-producing plasma cells is temporarily blunted, maternally protected pups do mount delayed protective humoral immunity after weaning. Fate-mapping of pre-existing B cells revealed that the RV-specific plasma cell pool originates from B cells imprinted at the time of virus exposure regardless of maternal protection. Our data challenges the dogma that maternal antibody is inhibitory and instead permits safe and efficacious immune education in the growing organism.