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The High-Affinity IgG Receptor, FcRI, Plays a Central Role in Antibody Therapy of Experimental Melanoma

¹ Immunotherapy Laboratory, Department of Immunology, University Medical Center Utrecht; ² Genmab, Utrecht, the Netherlands; and ³ Center for Human and Clinical Genetics, Leiden University Medical Center, Leiden, the Netherlands

Requests for reprints: Jan G.J. van de Winkel, Immunotherapy Laboratory, Department of Immunology, University Medical Center Utrecht, Lundlaan 6, KC.02.085.2, 3584 EA Utrecht, the Netherlands. Phone: 31-30-212-3100; Fax: 31-30-212-111; E-mail: j.vandewinkel{at}azu.nl.

We examined the role of FcR in antibody therapy of metastatic melanoma in wild-type and different FcR knock-out mice. Treatment of B16F10-challenged wild-type mice with TA99 antibody specific for the gp75 tumor antigen resulted in a marked decrease in numbers of lung metastases. Treatment of individual FcR knock-out mice revealed the high-affinity IgG receptor, FcRI (CD64), to represent the central FcR for TA99-induced antitumor effects. The potential of immune-modulating agents to further enhance the protective effect induced by monoclonal antibody (mAb) TA99 was examined in combination treatments consisting of mAb TA99 and a TLR-4 agonist, monophosphoryl lipid A (MPL). MPL did potently boost TA99 antibody-induced effects, and combination therapy was, again, found to be dependent on the presence of FcRI. (Cancer Res 2006; 66(3): 1261-4)

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