Passively acquired antibodies to respiratory syncytial virus impair the secondary cytotoxic T-cell response in the neonatal mouse.
Passively acquired antibody has been known since the 1940s to impair the secondary antibody response to the homologous antigen. However, the effect of passive immunity on the T-cell response is largely unknown. The results presented here demonstrate that monoclonal antibodies (Mabs) to respiratory syncytial virus (RSV), transferred in the mother's milk or injected directly, can reduce the generation of RSV-specific cytotoxic T-cell (Tc) precursors by the neonatal mouse; the development of influenza-specific Tc was unaffected. Both non-neutralizing and neutralizing antibodies, and Mabs directed against either the fusion (F) or G proteins of RSV, can impair the secondary Tc response. The ability of a given antibody to produce this impairment depends on its titre and its subclass, which determines its absorption from the gut by the neonate. These results are of interest in relation to virus infections in humans, such as RSV or measles, which are often contracted in the first 6 months of life, when maternal antibody is still present in high titre.
D000818:Animals; D000831:Animals, Newborn; D000911:Antibodies, Monoclonal / Q000276:immunology; D000914:Antibodies, Viral / Q000276:immunology*; D005260:Female; D007112:Immunity, Maternally-Acquired; D007074:Immunoglobulin G / Q000276:immunology; D051379:Mice; D008807:Mice, Inbred BALB C; D012136:Respiratory Syncytial Viruses / Q000276:immunology*; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology*
D000911:Antibodies, Monoclonal; D000914:Antibodies, Viral; D007074:Immunoglobulin G