Non-lytic antibodies in H-2-controlled resistance to acute infection with Trypanosoma cruzi.

1. Resistance to acute Trypanosoma cruzi infection in mice is a polygenic character with a major factor linked to the murine major histocompatibility system (H-2). We found that F1 hybrids A.CA(H-2f)/B10.Br(H-2k) between two susceptible strains are strongly resistant. 2. Resistant B10(H-2b) and A.SW(H-2s) animals survived 60 or more days after an intraperitoneal injection of 10(4) Tulahuén strain blood trypomastigotes. The specific antibody response of these individuals increased continuously up to 100 days or more. Parasitemia reached a peak at day 8 in all strains. Thereafter, the number of blood parasites in resistant animals showed an irregular but persistent decrease. 3. Susceptible congenic B10.Br and A.CA animals showed lower levels of specific anti-T. cruzi antibodies and an increase in parasitemia until death. B10.Br mice died 14 to 20 days after infection. A.CA animals were extremely susceptible, showing a sharp and sustained increase in parasitemia starting on day 12, followed by death no later than day 15 post-inoculation. 4. We found a significant correlation between IgG levels present in serum of resistant mice from 20 days on and protection against acute death. Whole immune anti-T. cruzi serum or its purified IgG class fraction neutralized T. cruzi inocula in vitro as shown by a significantly increased survival of recipient susceptible A.CA mice. 5. This IgG protective effect is independent of the protective effect mediated by the terminal activation of the complement cascade, since the parasites were inoculated with heat-inactivated immune sera and both recipient (A.CA) and donor (A.SW) strains lack C5.