Echinococcoses: a parasitic model for understanding allergic diseases?

Relationship between parasitic and allergic diseases has often been stresse d. Parasitic diseases do offer a model to study the role of those events th at may determine the final outcome of immune responses and the type of thei r effector stage. At first glance, the pathophysiological mechanisms involv ed in Echinococcus sp infections, hydatid cyst (cystic echinococcosis) and alveolar echinococcosis, appear quite different: IgE-dependent responses se em to be involved in the former and cell-mediated immunity in the latter Ho wever, an analysis of the cytokine profile in these two cestodoses shows th at, in both cases, Th1 responses are protective, and are present in "aborti ve" 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 patie nts, it seems that all known actors of the effector sell-mediated responses actually surround the parasitic cells but are somehow "paralysed", at leas t partially, by anti-inflammatory cytokines and other mediators such as nit ric oxide: hence the chronic evolution of the disease and all complications related to fibrosis and necrosis. Both are the results of an inefficient i mmune response deviated by the parasite and favoured by immunogenetic chara cteristics 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 "echinococc osis model" may be used to better understand the immune mechanisms involved both in the increase in allergic disorders in developed countries and in;m ixed-type allergic lesions" which associate cellular immunity and IgE-depen dent responses, such as atopic dermatitis. (C) 2001 Editions scientifiques at medicales Elsevier SAS.