Effective Phagocytosis and Killing ofCandida albicansvia Targeting FcγRI (CD64) or FcαRI (CD89) on Neutrophils

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Abstract
Invasive fungal infections are an increasing problem for immunocompromised patients. As an approach to improve targeting of polymorphonuclear leukocytes (PMNL) toward Candida albicans, the effect of bispecific antibodies (BsAbs) directed against C. albicans and either FcαRI or FcγRI was evaluated. Control PMNL and in vivo granulocyte colony-stimulating factor (G-CSF)—primed PMNL served as effector cells. A new radiometric killing assay for measuring candidacidal activity was developed to facilitate quantification of PMNL-mediated killing of C. albicans. BsAbs directed to either FcγRI (CD64) or FcαRI (CD89) on human PMNL effectively enhanced both phagocytosis and killing of C. albicans in vitro. Fungicidal activity triggered via FcγRI required in vivo priming with G-CSF, whereas FcαRI-mediated activity was not dependent on this growth factor. Furthermore, PMNL from human FcγRI-transgenic mice effectively phagocytosed and eliminated C. albicans in the presence of BsAbs. These results document the capacity of FcR-directed BsAbs and G-CSF to trigger antifungal immune responses.

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