FcR γ-Chain Dependent Signaling in Immature Neutrophils Is Mediated by FcαRI, but Not by FcγRI

Abstract

Neutrophil-mediated tumor cell lysis is more efficiently triggered by FcαRI (CD89), than by FcγRI (CD64). This difference is most evident in immature neutrophils in which FcγRI-mediated tumor cell lysis is absent. In this study, we show that FcR γ-chain-dependent functions (such as Ab-dependent cellular cytotoxicity and respiratory burst), as well as signaling (calcium mobilization and MAPK phosphorylation), were potently triggered via FcαRI, but not via FcγRI, in immature neutrophils. Internalization, an FcR γ-chain-independent function, was, however, effectively initiated via both receptors. These data suggest an impaired functional association between FcγRI and the FcR γ-chain, which prompted us to perform coimmunoprecipitation experiments. As a weaker association was observed between FcγRI and FcR γ-chain, compared with FcαRI and FcR γ-chain, our data support that differences between FcαRI- and FcγRI-mediated functions are attributable to dissimilarities in association with the FcR γ-chain.