Bakiri et al ship between the skin allergy and parasitic pathologies. Ir- respective of the abundant literature regarding the associa- tion between exposure to parasites and the enhancement of IgE response, no definite conclusions about the causality of the weak association between these findings and the low frequency of urticarial reactions are yet warranted. To shed some light into this question, this review is focused on the actual knowledge about parasites life cycle, interactions with host immunity, the influence on host behavior as well as the role of these factors on the urticaria and skin allergy. The Role of Host-parasite Interaction in the Relationship Parasitosis-Urticarial Reaction Th2 host response and parasites survival/development Parasites are designed by evolution to invade the host and survive in its organism until they are ready to reproduce [20]. They can release a variety of molecules that help them to penetrate the defensive barriers and avoid the immune at- tack of the host. In this respect, particularly interesting are enzymes and their inhibitors secreted by the parasites [13, 14, 20]. Thus, while serine-, aspartic-, cysteine-, and metal- loproteinases are involved in tissue invasion and extracel- lular protein digestion, helminths secrete serpins, aspins, and cystatins to inhibit proteinases, both of the host and their own. Proteinases and their inhibitors, as well as helminth homologues of cytokines and molecules containing phos- phorylcholine, influence the immune response of the host biasing it towards the “anti-inflammatory” Th2 type [13-15, 20]. Besides the eosinophilic infiltration, the IgE response as component of the Th2 profile is estimated to be a cornerstone of host defense during parasitoses [12-16, 21]. During parasitoses, the efficacy of the Th1 response may be superior to the Th2 one Current reports suggest that interaction between parasites and hostile immunity is more complex than previously es- timated. In this respect, the experimentally obtained data indicate that even hostile cytokines used for cell-cell com- munication can also be exploited by the parasite as clues to find suitable target organs [22]. In nematodes, the Th2 type response is affected by parasite dose [21]. For Trichi- uris muris infections, Th1-type immune responses occurred in animals given repeated low dose infections; latterly, the immune response developed into a protective Th2-type re- sponse. During Strongyloides ratti infections, the host im- mune response changes both qualitatively from a Th1- to a Th2-type immune response and the Th2-type response in- creases quantitatively with higher dose infections [21]. Fur- thermore, parasite survivorship was significantly negatively related to the concentration of parasite-specific IgG1 and IgA J Clin Med Res • 2010;2(6):247-255 [23, 24]. At the metacestode stage of Echinococcus infection, studies of the immune responses in the experimental murine model as well as in humans have shown that (i) cellular im- munity induced by a Th1-type cytokine secretion was able to successfully kill the metacestode at the initial stages of development; (ii) antigenic proteins and carbohydrates of the oncosphere/metacestode were able to interfere with antigen presentation and cell activation, leading to the production of IL-10 and other mediators by host lymphocytes and other immune cells, and therefore, to the inhibition of the effector phase of cellular immune reaction; and (iii) immunogenetic characteristics of the host were essential to this parasite- induced deviation of the immune response [25]. Regarding anisakiasis, acute symptoms are caused by an IgE-mediated allergic reaction in the gastrointestinal wall. Cuellar et al. demonstrated that anisakis antigens react with antibodies raised against vertebrate IL-4 [26]. With respect to schisto- somosis, most of the chronic patients presented a Th2 profile with low production of gamma interferon (IFN-γ) as com- pared to subjects resistant to this infection, while the inten- sity of infection favors the production of IL-10 [27]. In addi- tion, the blockade of IL-4 and IL-5 as well as the addition of the recombinant IL-10 significantly reduced the peripheral blood mononuclear cell proliferative response to soluble egg and adult worm antigens [28]. Meanwhile, experiments in mice have shown that the relative success of Giardia muris in completing its life cycle in a primary infection might be due, in part, to the stimulation of a Th2-type response. In contrast, a stronger Th1 response may lead to a better control of the primary infection [29]. These data suggest that IL-10 is an important cytokine in regulating the immune response and possibly controlling morbidity in human parasitoses, and that the production of IFN-γ may be associated with resis- tance to infection [28]. Taken together, these findings may suggest that hos- tile IgE/Th2 response has defensive effects, but the IgG/ Th1 type may also provide such qualities, which in some situations seem to be superior to the Th2 one. In vivo, the Th2 profile might be not simply a host-chosen reaction, but rather the most efficient permitted humoral response dur- ing host-parasite interaction. The fatal outcome in appar- ently immunocompetent patients due to multiorgan failure after Strongyloides stercoralis septicaemia following a short course of prednisolone therapy may lead to the suggestion that glucocorticoids may suppress the parasite-attenuated host immune defenses [30]. In our opinion, the Th2 devia- tion may permit parasites to invade the host organism, and to select specific organs or host cell types as predilection site to reside, maturate or even proliferate [13, 31, 32]. While many microparasites escape immune attack by antigenic variation or sequestration in specialized niches, helminths appear to thrive in exposed extracellular locations, such as the lymphatics, bloodstream, or gastrointestinal tract. Key events among the host cell population are dominance of the 248 Articles © The authors | Journal compilation © J Clin Med Res and Elmer Press™ | www.jocmr.org