Fifty-six (56) pigs were immunized against Taenia solium cysticercosis with antigens from Taenia crassiceps metacestodes, in a variety of protocols, and then challenged orally with Taenia solium proglottids or eggs. Results of immunization (expressed as individual parasite loads) ranged from significant reduction of parasite loads (host protection) to clear increase (parasite facilitation) in apparent relation to the immunogen dose, adjuvant employed and genetic background of the pigs. In all trials, however, immunized pigs harboured more damaged cysticerci than controls, indicating that immunization does induce some restrictions to parasite survival even if these are eventually overwhelmed by other parasite-promoting factors. Western blots in immunized-protected pigs indicated antigens of 242, 234, 118, 77, 55 and 45 kDa as possibly being involved in immunological protection.

Peritoneal infection with Taenia crassiceps cysticerci of naturally resistant (C57BL/10J and C57BL/6J) and susceptible (BALB/cAnN) mice induces a cellular immune depression. T-cell proliferation in response to concanavalin A (ConA) or anti-CD3 was significantly depressed in infected mice of all strains tested. However, in resistant mice, the diminished response to ConA was transient and animals recovered normal responsiveness at day 40, whereas susceptible mice remained suppressed throughout the 40 days of the experiment. In contrast, the proliferative response to anti-CD3 was lower in infected mice than in noninfected controls regardless of differences in natural susceptibility of the strains. Intraperitoneal injection of mice with a parasite extract also induced a depression of the response to ConA, although not as strong as that produced by the parasite itself. This depression is not due to direct effects by parasite antigens over host lymphocytes, as proliferation is not affected by the presence of cysticercal antigens added in vitro. Diminished interleukin-2 production during the parasitosis accounts at least in part for the diminished responses to ConA. A primary infection favors parasite establishment after a second challenge, pointing to the relevance of the immunodepression in generating a host environment favorable to the parasite.