Studies have shown that TES products exhibit an overlapping but not identical epitopes repertoire to those antigens expressed at the larval surface. The glycocalyx outside the epicuticle is recognized as a dynamic structure, which turns over quite rapidly and serves as a renewable source of large quantities of antigens. The major host responses to these antigens include a marked eosinophilia and hypergamma-globulinemia. Both eosinophils and IgE

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antibodies are associated with the expansion of the Th2 subset of T helper cells that secrete the cytokines, interleukin (IL)-4 and IL-5. There are reasons to believe that the antigens released from T. canis larvae favour the induction of Th2 cell population. On the other hand, the proportion of Th1 subset cells is less then normal during the infection, resulting in limited or no secretion of IL-2 and IFN-gamma (Del Prete et al. 1991, 1995).

Besides the immune responses mentioned earlier, the infective larvae elicit a production of specific IgG, IgM, IgA, and IgE isotype antibodies to TES. Interestingly, the specific IgM responses do not diminish over time, which may indicate a failure of isotype switching function or something antigenically unique about TES, or both (Bowman et al. 1987; Smith 1993).

Despite the paratenic host's response with both non-specific inflammatory and specific immune reactions, there is a prolonged survival of the larvae in tissues and granulomas. This phenomenon can, to some degree, be explained by immune evasion. In short-term acute infections, using immunohistochemistry Parson et al. (1986) demonstrated TES deposition in sinuous patterns suggestive of larval migration. In chronic infections, TES was localized within granulomas, both within the core of those containing larvae, or extracellularly within the inner rim of the collagen capsule of those in which neither larvae nor visible larval remnants were evident. These observations seem consistent with active shedding of TES as it is formed in the surface coat of the parasite. In this way the larvae are able to shed the host immune response, escape and re-migrate.

Several reports have demonstrated that in animals, which have been previously sensitized, a large proportion of migrating larvae will remain within the liver rather than continuing to migrate. Larval numbers imply that larvae are trapped in the liver rather than delayed in their migration. However, liver trapping does not protect the eyes or brain of sensitized mice from larval migration, nor does it result in larval killing (Parsons and Grieve 1990). Eosinophils seem not to be necessary for liver trapping as treatment of mice with antibody to IL-5 prevents both blood and tissue eosinophilia but does not affect liver trapping (Parsons et al. 1993). The biological significance of larval trapping is still unknown.

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