ArticleArthritis research & therapy2004
A proinflammatory role for Fas in joints of mice with collagen-induced arthritis.
Article in Arthritis research & therapy, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 31 citations in OpenAlex.
- Midline 1 associated with Fas signaling enhances murine antigen-induced arthritis.Frontiers in cell and developmental biology · 2025Article
- Apoptotic cell death in disease-Current understanding of the NCCD 2023.Cell death and differentiation · 2023Review
- TRAIL and FasL Functions in Cancer and Autoimmune Diseases: Towards an Increasing Complexity.Cancers · 2019Review
- CD95-ligand contributes to abdominal aortic aneurysm progression by modulating inflammation.Cardiovascular research · 2019Article
- Use of Lentiviral Particles As a Cell Membrane-Based mFasL Delivery System forFrontiers in immunology · 2017Article
- Treatment with LPS plus INF-γ induces the expression and function of muscarinic acetylcholine receptors, modulating NIH3T3 cell proliferation: participation of NOS and COX.British journal of pharmacology · 2014Article
- Role of Fas and Treg cells in fracture healing as characterized in the fas-deficient (lpr) mouse model of lupus.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2014Article
- Osteoblastogenesis from synovial fluid-derived cells is related to the type and severity of juvenile idiopathic arthritis.Arthritis research & therapy · 2012Article
- Identifying a major locus that regulates spontaneous arthritis in IL-1ra-deficient mice and analysis of potential candidates.Genetics research · 2011Article
- Targeting Fas in osteoresorptive disorders.Expert opinion on therapeutic targets · 2010Review
- Farber disease: clinical presentation, pathogenesis and a new approach to treatment.Pediatric rheumatology online journal · 2007Article
- Neutrophil apoptosis in autoimmunity.Journal of molecular medicine (Berlin, Germany) · 2006Review
- Perforin deficiency attenuates collagen-induced arthritis.Arthritis research & therapy · 2005Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Collagen-induced arthritis (CIA) is a chronic inflammatory disease bearing all the hallmarks of rheumatoid arthritis, e.g. polyarthritis, synovitis, and subsequent cartilage/bone erosions. One feature of the disease contributing to joint damage is synovial hyperplasia. The factors responsible for the hyperplasia are unknown; however, an imbalance between rates of cell proliferation and cell death (apoptosis) has been suggested. To evaluate the role of a major pathway of cell death - Fas (CD95)/FasL - in the pathogenesis of CIA, DBA/1J mice with a mutation of the Fas gene (lpr) were generated. The susceptibility of the mutant DBA-lpr/lpr mice to arthritis induced by collagen type II was evaluated. Contrary to expectations, the DBA-lpr/lpr mice developed significantly milder disease than the control littermates. The incidence of disease was also significantly lower in the lpr/lpr mice than in the controls (40% versus 81%; P < 0.05). However DBA-lpr/lpr mice mounted a robust immune response to collagen, and the expression of local proinflammatory cytokines such as, e.g., tumor necrosis factor alpha (TNF-alpha) and IL-6 were increased at the onset of disease. Since the contribution of synovial fibroblasts to inflammation and joint destruction is crucial, the potential activating effect of Fas on mouse fibroblast cell line NIH3T3 was investigated. On treatment with anti-Fas in vitro, the cell death of NIH3T3 fibroblasts was reduced and the expression of proinflammatory cytokines TNF-alpha and IL-6 was increased. These findings suggest that impairment of immune tolerance by increased T-cell reactivity does not lead to enhanced susceptibility to CIA and point to a role of Fas in joint destruction.
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