PRODUCTION OF AN INTERFERON-GAMMA HOMOLOG BY AN INTESTINAL NEMATODE -FUNCTIONALLY SIGNIFICANT OR INTERESTING ARTIFACT

Chronic infection is a prominent feature of many intestinal nematode i nfections in man and animals. It is also clear that in such situations host immunity is activated but is unable to induce a protective respo nse. A great deal of work has shown that genetic control of host immun ity contributes to the variation in worm burdens often observed in the held. 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 ha ve shown that parasite derived molecules share cross reactive epitopes with the host cytokine interferon-gamma using cytokine specific monoc lonal antibodies in ELISA, Western blotting and immunoprecipitation as says. Furthermore, the parasite molecules can be shown to bind to the interferon-gamma receptor and induce change in lymphoid cells similar to those induced by murine interferon-gamma. The functional activity o f the molecule in vivo remains to be determined. Previous studies have established that interferon-gamma is critical for progression to chro nic T. muris infection in mice and, therefore, it raises the distinct possibility that the production of an interferon-gamma homologue by th e 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.