Although IL-4R–dependent responses are necessary for rapid eosinophil-mediated primary immunity to establishing filarial larvae, we reveal that a layer of redundancy exists so that IL-4/13–independent and IL-5– and CCR3-dependent processes can compensate and more gradually exert immune killing to prefecund adult infections by mediation of a modified eosinophil recruitment. The gene discussed is CCR3; the disease is infection.