IFN-gamma-independent IgG2a production in mice infected with viruses and parasites

\After infection with some viruses and intracellular parasites, antibody pr oduction is restricted to IgG2a. We first observed that, whereas live virus es such as lactate dehydrogenase-elevating virus (LDV) or mouse adenovirus induced mostly an IgG2a response, a large proportion of antibodies produced against killed viruses were IgG1, This IgG1 antiviral response was suppres sed when live virions were added to inactivated viral particles. These resu lts indicate that the IgG2a preponderance is related to the infectious proc ess itself rather than to the type of antigen involved. Since IFN-gamma is known to stimulate IgG2a production by activated B lymphocytes and to be se creted after infection, we examined the role of this cytokine in the antibo dy isotypic distribution caused by LDV. Most IgG2a responses were relativel y unaffected in mice deficient for the IFN-gamma receptor or treated with a nti-IFN-gamma antibody. A similar IFN-gamma-independent IgG2a secretion was observed after infection with the parasites Toxoplasma gondii and Trypanos oma cruzi, However, the IFN-gamma-independent IgG2a production triggered by infection still required the presence of functional T-h lymphocytes. There fore, signal(s) other than IFN-gamma secretion may explain the T-h-dependen t isotypic bias in antibody secretion triggered by viruses and parasites.