Inhibition of murine fibrocyte differentiation by cross-linked IgG is dependent on FcRI.
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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 FcRs, and aggregated or cross-linked IgG inhibits fibrocyte differentiation. Mice have four different FcRs, and which of these, if any, mediate the cross-linked IgG effect on fibrocyte differentiation is unknown. We find that in mice, deletion of FcRI or the common signaling protein FcR significantly reduces the ability of cross-linked IgG or IgG2a to inhibit fibrocyte differentiation. Cells from FcRIIb/III/IV KO mice are still sensitive to cross-linked IgG, whereas cells from FcRI/IIb/III/IV KO mice are insensitive to cross-linked IgG. These observations suggest that IgG-mediated inhibition of fibrocyte differentiation is mediated by FcRs, with FcRI mediating most of the signaling.