The combination of cyclophosphamide treatment and Toxocara canis infection is known as an effective way of causing a high level of eosinophilia in mice. When this treatment was applied to congenitally anemic, mast cell-deficient W/Wv mice, eosinophil response was far less than that of their normal littermate +/+ mice. The degree of the defective eosinophil response in the peripheral blood of W/Wv mice was severer than that in the bone marrow. The defective eosinophil response of W/Wv mice was completely restored by bone marrow grafting 8 weeks prior to cyclophosphamide treatment and T. canis infection. The kinetics of the recovery of eosinophil response in the bone marrow of W/Wv mice after bone marrow grafting was faster than that in the peripheral blood. Chemotactic reactivity of eosinophils obtained from bone marrow or peritoneal cavity of W/Wv mice was essentially comparable to that of +/+ mice. These results suggest that, in addition to the production of eosinophils in the bone marrow, mast cell-derived factors play an important role in the mediation of peripheral blood eosinophilia.