Induction of autoimmune gastritis by neonatal thymectomy requires autoantibodies and is prevented by anti-FcγR antibodies.

The autoantibodies (auto-Abs) that are a hallmark of neonatally thymectomized (NTx) mice with autoimmune gastritis (AIG) have been poorly explored. We investigated their immune significance using B cell-deficient (B(-)) mice and found that B(-) mice are totally resistant to AIG but become susceptible to AIG after receiving bone marrow cells from B(+) mice. This susceptibility is most likely caused by the production of auto-Abs by B cells because B(-) pups also became susceptible to AIG when nourished by an AIG dam producing auto-Abs of the IgG class during the suckling period. NTx B(-) mice receiving purified IgG auto-Abs at this developmental stage similarly developed AIG. Auto-Abs probably act on antigen handling for antigen presentation because the treatment of NTx B(+) mice with anti-FcγR Abs prevented the development of AIG. Auto-Abs are indispensable for AIG development but are not sufficient because auto-Ab treatment did not increase AIG incidence in NTx B(+) mice above the baseline.