Maternal IgG and IgA Antibodies Dampen Mucosal T Helper Cell Responses in Early Life

To maintain a symbiotic relationship between the host and its resident intestinal microbiota, appropriate mucosal T cell responses to commensal antigens must be established. Mice acquire both IgG and IgA maternally; the former has primarily been implicated in passive immunity to pathogens while the latter mediates host-commensal mutualism. Here, we report the surprising observation that mice generate T cell-independent and largely Toll-like receptor (TLR)-dependent IgG2b and IgG3 antibody responses against their gut microbiota. We demonstrate that maternal acquisition of these antibodies dampens mucosal T follicular helper responses and subsequent germinal center B cell responses following birth. This work reveals a feedback loop whereby T cell-independent, TLR-dependent antibodies limit mucosal adaptive immune responses to newly acquired commensal antigens and uncovers a broader function for maternal IgG. [Display omitted] •Healthy mice make T-independent IgG2b and IgG3 Abs reactive to mucosal bacteria•Gut microbes elicit anti-commensal IgG antibodies via TLR signaling on B cells•Maternal transmission of IgG coordinates with IgA to limit mucosal T cell responses•Absence of maternal antibodies triggers a compensatory T-dependent immune response Maternally acquired, commensal-specific IgG antibodies coordinate with IgA to limit mucosal T cell responses and reinforce intestinal immunity in neonates.