Abstract
Relationship between parasitic and allergic diseases has often been stressed. Parasitic diseases do offer a model to study the role of those events that may determine the final outcome of immune responses and the type of their effector stage. At first glance, the pathophysiological mechanisms involved in Echinococcus sp infections, hydatid cyst (cystic echinococcosis) and alveolar echinococcosis, appear quite different: IgE-dependent responses seem to be involved in the former and cell-mediated immunity in the latter. However, an analysis of the cytokine profile in these two cestodoses shows that, in both cases, Th1 responses are protective, and are present in “abortive” forms of infection; conversely, Th2 responses characterised by IL-5 and especially IL-10 synthesis are the hallmarks of the “progressive” forms of infection, leading to the disease and its clinical complications. In patients, it seems that all known actors of the effector cell-mediated responses actually surround the parasitic cells but are somehow “paralysed”, at least partially, by anti-inflammatory cytokines and other mediators such as nitric oxide; hence the chronic evolution of the disease and all complications related to fibrosis and necrosis. Both are the results of an inefficient immune response deviated by the parasite and favoured by immunogenetic characteristics of the host. The IgE synthesis that results from the Th2 immune response also participate in the occurrence of clinical complications. The comparison between parasitic and allergic diseases, through the “echinococcosis model” may be used to better understand the immune mechanisms involved both in the increase in allergic disorders in developed countries and in “mixed-type allergic lesions” which associate cellular immunity and IgE-dependent responses, such as atopic dermatitis.
Published Version
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