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The host deploys a subset of immune responses to expel helminths, which differs depending on the nature of the helminth.Strongyloides venezuelensis , a counterpart of the human pathogenS. stercoralis , naturally infects rodents and has been used as an experimental model. Here we show that induction of immunoglobulin G (IgG) and IgE is a prerequisite for rapid expulsion ofS. venezuelensis during a primary infection. Activation-induced cytidine deaminase-deficient (AID−/− ) mice, which lack the ability to switch IgM to other isotypes, normally developed T-helper 2 (Th2) cells and intestinal mastocytosis after infection withS. venezuelensis . Although AID−/− mice expelledNippostrongylus brasiliensis normally, they required a much longer period to expelS. venezuelensis than wild-type (WT) mice. Adoptive transfers of immune sera fromS. venezuelensis -infected but notN. brasiliensis -infected mice restored the ability of AID−/− mice to promptly expelS. venezuelensis . Immune serum-derived IgG and IgE induced worm expulsion via Fc γ receptor III (FcγRIII) and Fc ε receptor I (FcεRI), respectively, and a mixture of IgG and IgE showed collaborative effects. Whereas FcγRIII−/− mice or FcεRIα−/− mice normally could expelS. venezuelensis , FcγRIII−/− mice, when their IgE was neutralized by anti-IgE, or FcεRIα−/− mice, when their IgG binding to FcγRIII was blocked by anti-FcγRIII, showed a markedly reduced ability to expelS. venezuelensis . These data reveal that IgG and IgE play redundant roles but act in concert to accelerateS. venezuelensis expulsion. Mast cell-deficient mice, even those equipped with immune serum-derived IgG or IgE, failed to expelS. venezuelensis promptly, suggesting that mast cells are cellular targets of IgG and IgE.

IgG and IgE Collaboratively Accelerate Expulsion of Strongyloides venezuelensis in a Primary Infection