Chronic infection is a prominent feature of many intestinal nematode infections in man and animals. It is also clear that in such situations host immunity is activated but is unable to induce a protective response. A great deal of work has shown that genetic control of host immunity contributes to the variation in worm burdens often observed in the field. There is increasing appreciation, however, of the capability of infectious agents themselves to modulate the host immune response and potentiate their own survival. Using an immunologically well defined model of intestinal nematode infection in mice (Trichuris muris) we have shown that parasite derived molecules share cross reactive epitopes with the host cytokine interferon-γ using cytokine specific monoclonal antibodies in ELISA, Western blotting and immunoprecipitation assays. Furthermore, the parasite molecules can be shown to bind to the interferon-γ receptor and induce change in lymphoid cells similar to those induced by murine interferon-γ. The functional activity of the molecule in vivo remains to be determined. Previous studies have established that interferon-γ is critical for progression to chronic T. muris infection in mice and, therefore, it raises the distinct possibility that the production of an interferon-γ homologue by the worm may be one mechanism whereby the parasite is able to interfere with the regulation of the host immune response and potentiate its own survival.