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J Leukoc Biol. 2014 Aug;96(2):275-82. doi: 10.1189/jlb.3AB0913-490RR. Epub 2014 Apr 21.

Inhibition of murine fibrocyte differentiation by cross-linked IgG is dependent on FcγRI.

Author information

  • 1Department of Biology, Texas A&M University, College Station, Texas, USA;
  • 2Department of Biology, Texas A&M University, College Station, Texas, USA; Department of Biochemistry and Cell Biology, Rice University, Houston, Texas, USA; and.
  • 3Department of Human Genetics, Leiden University Medical Center, Leiden, The Netherlands.
  • 4Department of Biology, Texas A&M University, College Station, Texas, USA; Department of Biochemistry and Cell Biology, Rice University, Houston, Texas, USA; and rgomer@tamu.edu.

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.

© 2014 Society for Leukocyte Biology.

KEYWORDS:

CD64; FcRγ; SAP; monocyte; pentraxin

PMID:
24752483
[PubMed - indexed for MEDLINE]
PMCID:
PMC4101091
[Available on 2015-08-01]
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