The aim of the studies was to identify the regulatory mechanisms that act at different levels of the ongoing immune response in BALB/c mice infected with intestinal nematode H. polygyrus. The role of TGF-beta during the course of H. polygyrus infection and an immunosuppressive action of the nematode against eosinophil response in allergic pulmonary inflammation has been studied. An attempt to identify the immunoregulatory proteins of the parasite has been performed as well. The obtained results proved: (1) for the first time the direct role of TGF-beta in the regulation of the immune response during helminth infections. Neutralization of TGF-beta in vivo increased concentration of IL-12, TNF-alpha and IL-10 in serum of infected mice and restored the control number of eosinophils in the intestinal mucosa. The mobilization of the immune response after neutralization of TGF-beta led to persistent decrease of nematode egg production and faster rejection of the worm from mouse intestine; (2) for the first time it was shown that the reduction of eosinophil number was due to the lower production of eotaxin and reduced expression of CCR3 receptor, playing an essential role in the chemotaxis of these leukocytes in Ova-related asthma; (3) significant decrease of T cell proliferation by one of the H. polygyrus protein fraction. With the use of mass spectrometry seven proteins have been identified: two heat shock proteins, disulfide isomerase, calreticulin, calumenin, fructose-bisphosphate aldolase, glyceraldehyde-3-phosphate dehydrogenase. From the bibliographic data it may be supposed that calreticulin could mediate the downregulation of lymphocytes proliferation. The fraction with calreticulin stimulated also production of specific IgE.