Probably due to their long common evolution with their hosts, parasites have developed an efficient strategy to escape the immune mechanisms their presence induces. Especially with helminths, these mechanisms have the advantage of limiting the infection at a level which favours the host, and therefore the parasite, survival. Three decades of research in the field of antischistosome immunity has revealed that a large panel of immune functions, involving nearly all immune cell types, several cytokines or cell mediators, and the participation of specific antibodies of various isotypes are required for the rapid and effective killing of infective larvae. In this context, antibodydependent cell cytotoxicity constitutes the mainstay of killing mechanisms against helminths, with a particular involvement of the IgE isotype. The cellular part of ADCC covers a large panel of inflammatory cells, from mononuclear phagocytes (macrophages and monocytes) to neutrophils, eosinophils, or blood platelets. It is difficult to assign to each participant its actual importance in the defence strategy of the immune system. The in vitro and ex vivo experiments have given a biased perspective of the involvement of each cell population, artificially amplifying their individual role. However, these investigations have allowed the demonstration of new functions for several inflammatory cell types, especially in the field of IgE responses, with a particular emphasis in allergic disorders.

This is particularly true for blood platelets, once thought to be exclusively involved in hemostasis and thrombosis, but now recognized as cells demonstrating a wide reactivity to soluble mediators and a complex metabolic behaviour beyond involvement in blood clotting or thrombus formation.