Human Fc Receptors: Critical Targets in the Treatment of Autoimmune Diseases and Transplant Rejections

Aberrant expression of FcγRIIIA (CD16) contributes to the development of atherosclerosis

“…Of them, FcγRIIIA (CD16) is a transmembrane subtype and mainly expressed on monocytes (Masuda et al, 2009). Previous studies on FcγRIIIA have extensively focused on the relationship between gene polymorphisms or gene expression differences and diseases (Abe et al, 2005;Ivan and Colovai, 2006;Kawanaka et al, 2002). In agreement with previous studies, our recent study also suggested that increased mRNA expression and protein level of FcγRIIIA were correlated to CHD development, and FcγRIIIA was mainly expressed on monocytes (data not shown).…”

Fc receptor engagement mediates differentiation of cardiac fibroblast precursor cells

“…There is significant evidence in the literature of a variety of changes induced by TEM in both mononuclear and neutrophil cell populations (25,26). Similarly, although the role of FcR in modulating monocyte phenotypes has been described previously (7,8), their role in monocyte-tofibroblast transition is unique, as is the fact that the FcR modulation must occur before TEM. A recent study described endothelial cells as a source of cardiac fibroblast formation via endothelial-to-mesenchymal transition (27).…”

“…Therefore, the current study provides strong evidence for a regulatory role of ligands that mediate monocyte-to-fibroblast transition through activating FcRs. Activation of FcRs is already a well known mechanism of modulating monocyte/macrophage phenotype, so there is a precedent that such a mechanism also might mediate monocyteto-fibroblast transition (7,8).…”

“…SAP is a ligand for activating FcRs (9). Most activating FcRs associate with a common membranesignaling component termed FcR␥ chain protein that contains an immunoreceptor tyrosine-based activation motif (ITAM) to exert their effects (7,8).…”

Cytokine Release After Treatment With Rituximab in Renal Transplant Recipients

“…4 The observation that polymorphisms in the FcγRIIIa gene affect the effectiveness of RTX indicates that antibody-dependent cellular cytotoxicity plays an important role. 5 Natural killer (NK) cells express the Fc receptor FcγRIIIa (CD16) which has a high affinity for binding to immunoglobulin G (IgG)1, 6 the isotype of RTX. FcγRIIIa appears in 2 allelic forms that differ by the amino acid on position 158.…”