The ambiguous role of immunity in echinococcosis: protection of the host or of the parasite?

In Echinococcus infection, at the metacestode stage, studies of the immune responses in the experimental murine model as well as in humans have shown that (1) cellular immunity induced by a Th1-type cytokine secretion was able to successfully kill the metacestode at the initial stages of development; (2) antigenic proteins and carbohydrates (and perhaps non-antigenic, mitogenic components) of the oncosphere/metacestode were able to interfere with antigen presentation and cell activation so that host lymphocytes and other immune cells could produce cytokines (especially IL-10) and other mediators able to inhibit the effector phase of cellular immune reaction; and (3) immunogenetic characteristics of the host were essential to this parasite-induced deviation of the immune response. In E. multilocularis infection, a combined Th1 and Th2 cytokine profile appears crucial for prolonged metacestode growth and survival. It may be hypothesized that Th1 cytokines promote the initial cell recruitment around the metacestode and are involved in the chronicity of the cell infiltrate leading to a fully organized periparasitic granuloma and its consequences, fibrosis and necrosis. The Th2 cytokines, on the other hand, could be responsible for the inhibition of a successful parasite killing especially because of the 'anti-inflammatory' potency of IL-10. This combination of various arms of the immune response results in a partial protection of both Echinococcus metacestode and host. However, it may also be considered responsible for several complications of the disease. The Th2-related IgE synthesis and mast cell activation, well known to be responsible for anaphylactic reactions in cystic echinococcosis, are more rarely involved in 'allergic' complications in alveolar echinococcosis (AE). However, the partial but chronic effects of the efficient Th1-related cellular immune response are responsible for cytotoxic events which both help metacestode growth and dissemination and lead to the central necrosis of the lesions and clinical complications of AE. Moreover, the Th-1 response is responsible for the major and irreversible fibrosis which leads to bile duct and vessel obstruction. In addition, the peri-parasitic fibrosis may be one of the reasons for the relative lack of efficacy of antiparasitic drugs. Modulation of the host immune response, by using Interferon alpha for instance, may be a new tool to generate an effective immune response against the parasite and to prevent AE and its complications.