Infection with Trichinella spiralis in mice generates Th-2 mediated response, which controls effector mechanism operating in the intestine. It is associated with a pronounced intestinal mastocytosis, eosinophilia and destruction of intestinal epithelial layer during expulsion of parasite from the gut. It is believed that protection is dependent on non-specific inflammatory reaction mediated by mast cells. Furthermore, the higher serum levels of parasite specific IgG1 and IgG2a and also mucosal IgA response were related to the course of infection. Inhibition of humoral and cellular immune responses using ketotifen as anti-allergic compound, resulted in the greater worm burden and worm size, but not in the significant prolongation of intestinal phase. Moreover, in treated mice epithelial layer of the gut was protected from destruction provoked by the nematode. As interaction between effector leukocytes and antibodies were not effective it was proposed that other mechanisms, not related to hypersensitivity or conventional inflammatory response regulated the level of infection. The immunological and physiological phenomenons are discussed in terms of events associated with protection to the parasite. Possibly, immunoregulatory capasity of the nematode is involved in the induction of multiple mechanisms operated during infection.