There is increasing evidence that helminth infections can protect the host against Th2-mediated allergic pathologies, even though helminths themselves are strong Th2 inducers. In murine model systems, alleviation of allergy is not achieved through immune deviation to Th1, but is linked to expansion of regulatory T cell activity. Parasite infection does not prevent allergen sensitisation, but restricts the Th2 effector phase responsible for inflammation. Suppression of allergic inflammation can be transferred by Treg phenotype cells from an infected, allergen-naive animal to an uninfected, sensitized recipient. Patent allergy in humans is also known to be modulated by helminth infections, suggesting that a similar regulatory network may be controlling immunopathologic disease in man.
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