| First Author | Pilling D | Year | 2014 |
| Journal | J Leukoc Biol | Volume | 96 |
| Issue | 2 | Pages | 275-82 |
| PubMed ID | 24752483 | Mgi Jnum | J:219453 |
| Mgi Id | MGI:5620850 | Doi | 10.1189/jlb.3AB0913-490RR |
| Citation | Pilling D, et al. (2014) Inhibition of murine fibrocyte differentiation by cross-linked IgG is dependent on FcgammaRI. J Leukoc Biol 96(2):275-82 |
| abstractText | 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 FcgammaRs, and aggregated or cross-linked IgG inhibits fibrocyte differentiation. Mice have four different FcgammaRs, and which of these, if any, mediate the cross-linked IgG effect on fibrocyte differentiation is unknown. We find that in mice, deletion of FcgammaRI or the common signaling protein FcRgamma significantly reduces the ability of cross-linked IgG or IgG2a to inhibit fibrocyte differentiation. Cells from FcgammaRIIb/III/IV KO mice are still sensitive to cross-linked IgG, whereas cells from FcgammaRI/IIb/III/IV KO mice are insensitive to cross-linked IgG. These observations suggest that IgG-mediated inhibition of fibrocyte differentiation is mediated by FcgammaRs, with FcgammaRI mediating most of the signaling. |
