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. 2016 Oct 24;7:433. doi: 10.3389/fimmu.2016.00433

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Copyright © 2016 Valenzuela, Hickey and Reed.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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FcγR-mediated effector functions. (A) Monocytes and neutrophils express FcγRs, which bind preferentially to different IgG subclasses. FcγR cross-linking by myeloid cells induces activation and mediates antibody-dependent cell-mediated cytotoxicity (ADCC), phagocytosis (ADCP), and augments recruitment of leukocytes from the blood. In general, IgG1 and IgG3 efficiently bind to most FcγR isoforms expressed by monocytes and neutrophils. IgG4 can bind quite well to FcγRI (CD64), and IgG2 is bound by an allelic variant of FcγRIIa (CD32a, H131). (B) NK cells express FcγRIII (CD16). Engagement of FcγRIII by antibody-coated target cells induces ADCC via degranulation and release of perforin/granzyme. Cross-linking of FcγRIII on NK cells also upregulates the inflammatory cytokines IL-12, IFNγ, and TNFα.