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We hypothesize that the Th2 cytokine‐induced Sm‐specific IgE promotes potent, Sm‐specific, atopic effector responses and Sm elimination from the host, and also cross‐reactive responses to some allergens, resulting in positive Sm‐allergy associations. By contrast, Sm‐specific IL‐10, IgG4 and/or nonspecific polyclonally stimulated IgE inhibit these allergy‐related outcomes. White and shaded arrows denote promotion and inhibition, respectively
