Unlike other eukaryotic cells, Trypanosoma lewisi forms caps at 0 degrees C when incubated with rabbit immunoglobulin G(IgG) directed against surface IgG from the rat host. The host IgG, which is specific for parasite antigens, probably does not cause capping of these antigens in vivo, since trypanosomes treated with Fab fragments directed against rat IgG are uniformly labeled and do not cap at 0 degrees C or 37 degrees C.

To test the hypothesis that the rapid immune response of rats to Trypanosoma lewisi is elicited by prior exposure to cross-reacting environmental antigens, the early immune response to infection with this nonpathogenic protozoan was studied in germ-free and conventional rats. In germ-free rats, initial levels of both IgG and IgM were significantly lower than those of conventional rats. After infection, the germ-free rats made more immunoglobulins of both classes, and made them more quickly, than did conventional rats. Trypanosome-specific antibodies appeared earlier and in higher titers in the germ-free rats. Because they lacked intestinal microflora, it is unlikely that the germ-free rats' responses had been primed; thus, these observations indicated that the conventional rats' responses to some trypanosome antigens had been down-regulated by their prior exposure to environmental antigens. However, protective antibodies that inhibited parasite reproduction (ablastin) may have been primed, because these appeared in sera 2 days earlier in conventional rats. Despite much lower rates of production of trypanosome-specific antibodies, the conventional rats had the same peak parasitemias and times to crisis as germ-free rats. Thus it is apparent that protective immunity to this nonpathogenic parasite is not down-regulated by prior exposure to environmental antigens, as would be predicted.