Abstract
Previous reports demonstrated that cyclophosphamide (Cy) enhances two Fcγ receptor (FcγR) mediated functions: antibody-dependent cellular cytotoxicity (ADCC) and phagocytosis. In this paper we examine the mechanisms whereby Cy modifies the cytotoxic capacity of mouse splenocytes. The results indicate that the observed augmentation of ADCC could not be attributed to a higher proportion of macrophages and/or polymorphonuclear leukocytes (PMN), but rather to an enhanced activity per effector cell. Binding studies showed that this augmentation was associated with an increased number, but not an increased avidity of FcγR sites. The possibility that the enhanced FcγR expression by Cy may result in the alteration of other FcγR-mediated functions is discussed.
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