Fc gamma receptor and Neonatal Fc receptor (FcγR / FcRn)

The Fc gamma receptors (FcγRs) and the neonatal Fc receptor (FcRn) are the primary receptors responsible for mediating the biological effects and pharmacokinetics of immunoglobulin G (IgG) (nih.gov, wikipedia.org). FcγRs are a family of cell-surface proteins, including FcγRI (CD64), FcγRII (CD32), and FcγRIII (CD16), expressed on various immune cells that link the adaptive immune system to innate effector functions such as phagocytosis and antibody-dependent cellular cytotoxicity (ADCC) (nih.gov, acrobiosystems.com). In contrast, FcRn is a structurally distinct MHC class I-like molecule encoded by the FCGRT gene that functions as a homeostatic regulator, protecting IgG and albumin from lysosomal degradation and extending their serum half-life (nih.gov, patsnap.com). In autoimmune diseases, these receptors are targeted to either clear pathogenic autoantibodies via FcRn blockade or modulate aberrant immune activation via FcγR signaling (nih.gov, delveinsight.com). Therapeutic strategies include monoclonal antibodies like nipocalimab and engineered Fc fragments like efgartigimod, which are designed to selectively interact with these receptors to treat conditions such as myasthenia gravis and immune thrombocytopenia (nih.gov, patsnap.com). Together, these receptors represent critical nodes for controlling antibody-mediated immunity and optimizing the performance of therapeutic antibodies (nih.gov, frontiersin.org).

Other names

Fc gamma receptor familyNeonatal Fc receptorFcRnFcγRBrambell receptorIgG Fc receptorsCD64CD32CD16FCGRTFCGR family

FcRn inhibitors bind to the neonatal Fc receptor to block the recycling of IgG, thereby increasing the catabolism of pathogenic autoantibodies (nih.gov, patsnap.com). FcγR-targeted therapies modulate immune responses by either activating effector functions like ADCC and phagocytosis through activating receptors (FcγRI, III) or by suppressing immune activation through the inhibitory receptor FcγRIIB (nih.gov, acrobiosystems.com).