Echinococcosis.

Abstract

Hydatids, the intermediate stages, or metacestodes, of the tapeworm genus, Echinococcus, present a major immunological problem; they survive, grow and metastasize in immunized hosts which are protected against reinfection and possess effector mechanisms capable of killing the parasite. Explanations for this state of concomitant immunity have been made from investigations of avoidance strategies, genetics and quantitative hydatid growth. The latter study suggests that the host-parasite relationship is sustained as a dynamic equilibrium between parasite growth and acquired immunity, the balance being subject to mutual regulation and including the possibility of spontaneous rejection of the parasite. Two immunoregulatory, or cytokine-like, factors have been detected in hydatids of Echinococcus spp. One appears to be a mediator of the previously reported mitogenic effects of hydatids. Recent evidence has linked these effects to generation of T-suppressor populations. The second factor interferes with the interaction of macrophages and T-cells, mimics the effect of metacestode infection in impairing the accessory action of macrophages in lymphoproliferative responses, and is suppressive for rosette-forming cell responses against third-party antigens. It is suggested that these factors form part of a primary homeostatic mechanism regulating hydatid growth and immunity.