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Enhancement of Polymorphonuclear Cell-mediated Tumor Cell Killing on Simultaneous Engagement of FcRI (CD64) and FcRI (CD89)¹

Departments of Cell Biology/Immunology and Surgical Oncology, Vrije Universiteit, Amsterdam, the Netherlands [M. v. E.]; Department of Immunology [A. B. v. S., H. V., G. H., J. G. J. v. d. W.], Medarex Europe [A. B. v. S.], and Genmab [J. G. J. v. d. W.], University Medical Center Utrecht, Utrecht, the Netherlands; and Department of Pathology, Faculty of Veterinary Medicine, Utrecht, the Netherlands [E. v. G.]

Antibodies can efficiently induce antitumor responses via recruitment of Fc receptor-bearing cytotoxic cells. Polymorphonuclear (PMN) cells represent attractive effector cells for antibody-directed immunotherapy. This, because activated PMN cells coexpress the class I receptors for IgG (FcRI, CD64) and IgA (FcRI, CD89), which are potent cytotoxic trigger molecules. Both receptors, however, require the FcR chain for signaling. In this study, we show that FcRI and FcRI can trigger function independently of one another and do not cross-compete for the FcR chain. FcRI proved more efficient in initiating early signaling events and effector functions, such as redirected tumor cell killing and generation of superoxide. In addition, simultaneous engagement of FcRI and FcRI resulted in enhanced tumor cell lysis. These data support the development of concepts in which both FcRI and FcRI on PMN cells are targeted for tumor therapy.

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