Mast cells, eosinophils and antibody-mediated cellular cytotoxicity are not critical in resistance to Trichuris muris.

The murine intestinal nematode Trichuris muris provides an invaluable model of human infection with T. trichiura. Hence, analysis of the immunological responses in the mouse may elucidate the mechanisms of immunity to trichuriasis in man. The work described here investigates the roles of eosinophils, mast cells and antibody-dependent cell-mediated cytotoxicity (ADCC) in the elimination of T. muris from the host gut. Following ablation of IL-5, and hence eosinophilia, mice usually resistant to T. muris infection remained so. Further, blocking the stem cell factor receptor, c-kit, to facilitate complete ablation of mast cells over the period of parasite expulsion in resistant mice had no effect on the development of protective immunity. Therefore it can be deduced that eosinophils and mast cells are not critical in resistance. In addition to these studies, the role of antibody-mediated cellular cytotoxic mechanisms was investigated via the analysis of an infection time course in Fc gamma R-/- mice. These animals, on a resistant background, were fully immune and expelled the parasites before development of the adult stage. Thus this model provides evidence against a major role for ADCC in resistance to infection with T. muris. The studies described here have eliminated some of the major effector mechanisms traditionally associated with helminth infection, and work continues to elucidate the critical immune responses associated with resistance.