ArticleThe American journal of pathology2003
FcgammaRI up-regulation induced by local adenoviral-mediated interferon-gamma production aggravates chondrocyte death during immune complex-mediated arthritis.
Article in The American journal of pathology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 30 citations in OpenAlex.
- An aptamer specifically targeting mCRP ameliorates experimental arthritis.Journal of orthopaedic translation · 2025Article
- Osteoimmunology in Osteoarthritis: Unraveling the Interplay of Immunity, Inflammation, and Joint Degeneration.Journal of inflammation research · 2025Review
- Ageing and interferon gamma response drive the phenotype of neutrophils in the inflamed joint.Annals of the rheumatic diseases · 2022Article
- Promising Therapeutic Targets for Treatment of Rheumatoid Arthritis.Frontiers in immunology · 2021Review
- Targeting IgG in Arthritis: Disease Pathways and Therapeutic Avenues.International journal of molecular sciences · 2018Review
- Translational mini-review series on Th17 cells: are T helper 17 cells really pathogenic in autoimmunity?Clinical and experimental immunology · 2010Review
- Lessons from animal models of arthritis over the past decade.Arthritis research & therapy · 2009Review
- Amplifying elements of arthritis and joint destruction.Annals of the rheumatic diseases · 2007Review
- Toll-like receptor 4 induced FcgammaR expression potentiates early onset of joint inflammation and cartilage destruction during immune complex arthritis: Toll-like receptor 4 largely regulates FcgammaR expression by interleukin 10.Annals of the rheumatic diseases · 2007Article
- High synovial expression of the inhibitory FcgammaRIIb in rheumatoid arthritis.Arthritis research & therapy · 2007Article
- The complex role of Fcgamma receptors in the pathology of arthritis.Springer seminars in immunopathology · 2006Review
- Dendritic cells from patients with rheumatoid arthritis lack the interleukin 13 mediated increase of Fc gamma RII expression, which has clear functional consequences.Annals of the rheumatic diseases · 2005Article
- Local IL-13 gene transfer prior to immune-complex arthritis inhibits chondrocyte death and matrix-metalloproteinase-mediated cartilage matrix degradation despite enhanced joint inflammation.Arthritis research & therapy · 2005Article
- NADPH-oxidase-driven oxygen radical production determines chondrocyte death and partly regulates metalloproteinase-mediated cartilage matrix degradation during interferon-gamma-stimulated immune complex arthritis.Arthritis research & therapy · 2005Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Using various FcgammaR-deficient mice, we have obtained suggestive evidence that FcgammaRI on macrophages is responsible for severe cartilage destruction during arthritis mediated by immune complexes (ICs). This role of FcgammaRI is pronounced in the presence of activated Th1 cells and a likely Th1 cell-derived cytokine mediating up-regulation of FcgammaRI expression is interferon (IFN)-gamma. We now investigated whether local overexpression of IFN-gamma using an adenoviral vector is able to elevate cartilage destruction during experimental immune complex-mediated arthritis (ICA) and to what extent this process is FcgammaRI-mediated. IFN-gamma overexpression during ICA had no significant effect on the total cell mass infiltrating the knee joint. However, a higher percentage of macrophages expressing markers for a proinflammatory phenotype was found and these macrophages were situated in close proximity of the cartilage surface. Interestingly, cartilage destruction as studied by matrix metalloproteinase (MMP)-mediated proteoglycan damage (VDIPEN expression), chondrocyte death, and erosion was significantly increased. This effect of IFN-gamma was only found in the presence of ICs, as IFN-gamma overexpression during zymosan-induced arthritis, which is not IC-dependent, did not lead to severe cartilage destruction. These results imply a crucial role for ICs and the IgG-binding receptors in the aggravation of cartilage damage by IFN-gamma. Local overexpression of IFN-gamma induced increased FcgammaRI mRNA levels in synovium. To study whether this up-regulation of FcgammaRI mediates aggravation of cartilage destruction, ICA was raised in FcgammaRI(-/-) and their wild-type controls. IFN-gamma resulted in elevated VDIPEN expression, which was still present in FcgammaRI(-/-). Of great interest, chondrocyte death remained low in FcgammaRI(-/-). These results indicate that IFN-gamma overexpression deteriorates cartilage destruction in the presence of ICs and that FcgammaRI is crucial in the development of chondrocyte death.
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