The role of cytophilic IgG3 antibody in T cell-mediated resistance to infection with the extracellular bacterium, Pseudomonas aeruginosa

Previous studies have demonstrated that T lymphocytes from mice immunized with a high m.w. polysaccharide Ag from Fisher-Devlin immunotype I Pseudomonas aeruginosa can adoptively transfer protection against challenge with the homologous bacterial strain to susceptible mice. This T cell-mediated resistance has been found to be B cell dependent, although serum from immunized mice is incapable of passively transferring protection to nonimmune mice. The current studies demonstrate that T cells from immunized mice possess receptors that permit them to be adsorbed to IgG3-secreting hybridomas, but not to IgM-secreting hybridomas. Cross-linking of antibody on the surface of immune T cells results in release of a soluble factor that inhibits bacterial growth. Treatment of T cells to remove cytophilic antibody eliminates their ability to adoptively transfer protection to nonimmune mice, and the protective ability can be restored by co-incubating the T cells with monoclonal P. aeruginosa-specific IgG3 antibody before adoptive transfer to nonimmune mice. These observations are consistent with a model in which T lymphocytes from immunized mice are activated by cross-linking of FcR for IgG3 to secrete an antibacterial lymphokine. The ability of IgG3 at low antibody concentrations to act synergistically with T lymphocytes to inhibit bacterial growth could explain the evolutionary selection of this antibody isotype as the predominant subclass of IgG secreted in response to bacterial capsular polysaccharide Ag.