Effect of genetic modification of antibody responsiveness on resistance to Toxoplasma gondii infection.
Resistance to Toxoplasma gondii infection was studied in the high (H/f) and low (L/f) antibody responder lines of mice that were selected on the basis of quantitative antibody responsiveness to the flagellar antigen of Salmonella (selection III). No interline difference was observed in resistance to a highly virulent strain of T. gondii. In contrast, H/f mice were much more resistant than L/f mice to a moderately virulent strain of T. gondii: a 5000-fold difference in terms of the 50% lethal dose was found. The degree of resistance in (H/f X L/f)F1 hybrids was intermediate compared with that in parental lines for both mortality and survival time. The antibody titers to Toxoplasma antigens measured during the course of the infection were significantly higher in H/f than in L/f mice. This interline difference was underestimated because parasite multiplication occurs faster in L/f mice, which increases antigenic stimulation. The stronger resistance of H/f mice is probably due to their higher capacity of antibody production in the course of infection.
D000818:Animals; D000917:Antibody Formation; D000953:Antigens, Protozoan / Q000276:immunology; D005260:Female; D005802:Genes, MHC Class II; D007113:Immunity, Innate; D008297:Male; D051379:Mice; D010586:Phagocytes / Q000469:parasitology; D014122:Toxoplasma / Q000276:immunology* / Q000472:pathogenicity; D014124:Toxoplasmosis, Animal / Q000235:genetics / Q000276:immunology*; D014774:Virulence
D000953:Antigens, Protozoan