By treating IL-4Rα−/− mice serially with anti-CCR3 Ab or introducing a compound deficiency in CCR3 within IL-4Rα−/− mice, residual eosinophilia was ablated, and susceptibility to chronic adult Brugia malayi infection was established, promoting a functional role for CCR3-dependent eosinophil influx in immune control in the absence of IL-4/IL-13–dependent immune mechanisms. The gene discussed is IL13; the disease is Increased total eosinophil count.