Although T(H)2 cytokine involvement in allergy makes these cytokines attractive therapeutic targets, they protect against ectoparasites and gastrointestinal worms and suppress inflammation induced by T(H)1 cytokines. T(H)2 cytokines induce mastocytosis, eosinophilia, IgE synthesis, and mucus production. Each element of this response protects against some worms; however, different worms are protected against by different elements of the total response. The induction of the entire response by most parasitic worms suggests that it is safer for the immune system to make a stereotyped worm-protective response than to attempt to match a more specific response to a particular worm. In contrast, the reciprocal antagonism between T(H)1 and T(H)2 cytokines suggests that it is safer for the immune system to limit immunopathology by suppressing inflammatory effector mechanisms not required for host protection against a particular pathogen class than to make an all-purpose inflammatory response. This, in turn, implies that innate immunity can distinguish different classes of parasites (eg, worms vs protozoa) but has limited ability to distinguish individual parasites within a class (eg, different worms). Although these considerations suggest that T(H)2 cytokine antagonists may increase the risk and severity of worm infections and T(H)1 cytokine-mediated inflammatory disorders, such therapy should be relatively safe if it is restricted to areas in which worm infections are rare and commonsense precautions are taken to minimize the risk of inducing T(H)1 cytokine-related inflammatory disease.