IgE-mediated host defense mechanism during Strongyloides venezuelensisinfection

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Activation-induced cytidine deaminase-deficient (AID-/-) mice, lacking the ability to switch IgM to other isotypes, required much longer period to expel S.venezuelensis than wild-type (WT) mice. Adoptive transfers of immune sera from S. venezuelensis-infected mice restored AID-/- mice to promptly expelled S.venezuelensis. Immune serum-derived IgG and IgE induced worm expulsion via Fc γ receptor III (FcγRIII) and Fc ε receptor I (FcεRI), respectively. IgG and IgE played redundant roles but acted in concert to promote S.venezuelensis expulsion. My findings also suggest that mast cells are cellular targets of IgG and IgE.