Inhibition of murine fibrocyte differentiation by cross‐linked IgG is dependent on FcγRI. Issue 2 (21st April 2014)

• Record Type: Journal Article
• Authors: Pilling, Darrell; Crawford, Jeffrey R.; Verbeek, J. Sjef; Gomer, Richard H.
• Is Part Of: Journal of leukocyte biology. Volume 96:Issue 2(2014)
• Page Start: 275
• Page End: 282
• Publication Date: 2014-04-21
• Subjects: monocyte -- SAP -- CD64 -- FcRγ -- pentraxin; Leucocytes -- Periodicals; Reticulo-endothelial system -- Periodicals; 571.96
• DOI: 10.1189/jlb.3AB0913-490RR
• Languages: English
• ISSNs: 0741-5400

Abstract

Abstract : FcγRI (CD64) mediates the inhibitory effects of cross‐linked IgG on murine fibrocytes. Abstract : Monocyte‐derived, fibroblast‐like cells, called fibrocytes, participate in wound‐healing and the formation of fibrotic lesions. Aggregated or cross‐linked IgG are key effectors in infections, autoimmune diseases, anaphylaxis, and immunotherapy. Cells, including monocytes and fibrocytes, bind IgG using FcγRs, and aggregated or cross‐linked IgG inhibits fibrocyte differentiation. Mice have four different FcγRs, and which of these, if any, mediate the cross‐linked IgG effect on fibrocyte differentiation is unknown. We find that in mice, deletion of FcγRI or the common signaling protein FcRγ significantly reduces the ability of cross‐linked IgG or IgG2a to inhibit fibrocyte differentiation. Cells from FcγRIIb/III/IV KO mice are still sensitive to cross‐linked IgG, whereas cells from FcγRI/IIb/III/IV KO mice are insensitive to cross‐linked IgG. These observations suggest that IgG‐mediated inhibition of fibrocyte differentiation is mediated by FcγRs, with FcγRI mediating most of the signaling.