ArticleFrontiers in immunology2022
Inflammatory activation of the FcγR and IFNγR pathways co-influences the differentiation and activity of osteoclasts.
Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 3 citations in OpenAlex.
- Article
- Systemic regulation of rheumatoid arthritis by mesenchymal stem cells: from immune homeostasis to microbiota modulation.Frontiers in immunology · 2026Review
- Elevated cytokines in osteoporotic blood correlate with immune microenvironment shifts and dysregulated circRNA profiles.Frontiers in immunology · 2026Article
- Osteoporosis: interferon-gamma-mediated bone remodeling in osteoimmunology.Frontiers in immunology · 2024Review
- Lacking ARHGAP25 mitigates the symptoms of autoantibody-induced arthritis in mice.Frontiers in immunology · 2023Article
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Authors and funding
7 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Osteoclasts are polykaryons formed by cell-cell fusion of highly motile progenitors of the myeloid lineage. Osteoclast activity can preserve skeletal strength and bone homeostasis. However, osteoclasts are responsible for bone destruction in rheumatoid arthritis (RA). Fc receptors activated by IgG immune complexes (IC) can boost osteoclast differentiation and bone loss in the course of RA. In contrast, interferon (IFN) γ secreted by immune cells blocks osteoclast activation. Despite their hypothetical importance in the regulation of osteoclast differentiation in RA, the interconnection between the two pathways has not been described so far. Here, we show by total internal reflection fluorescence (TIRF) microscopy that FcγR3 and IFNγ receptor (IFNγR) locate at close vicinity to each other on the human osteoclast surface. Moreover, the average distance increases during the differentiation process. Interestingly, FcγR and IFNγR activation shapes the position of both receptors to each other. Surprisingly, the inhibitory action of IFNγ on
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