ArticleThe Journal of clinical investigation1997
Amelioration of collagen-induced arthritis by CD95 (Apo-1/Fas)-ligand gene transfer.
Article in The Journal of clinical investigation, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
43 citing papers in PubMed, 197 citations in OpenAlex.
- A DNA origami device spatially controls CD95 signalling to induce immune tolerance in rheumatoid arthritis.Nature materials · 2024Article
- Article
- Pancreatic islets engineered with a FasL protein induce systemic tolerance at the induction phase that evolves into long-term graft-localized immune privilege.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2020Article
- Use of Lentiviral Particles As a Cell Membrane-Based mFasL Delivery System forFrontiers in immunology · 2017Article
- The tumour necrosis factor/TNF receptor superfamily: therapeutic targets in autoimmune diseases.Clinical and experimental immunology · 2011Article
- Harnessing programmed cell death as a therapeutic strategy in rheumatic diseases.Nature reviews. Rheumatology · 2011Review
- Modulation of collagen-induced arthritis by adenovirus-mediated intra-articular expression of modified collagen type II.Arthritis research & therapy · 2010Article
- MHC-dependent desensitization of intrinsic anti-self reactivity.Cancer immunology, immunotherapy : CII · 2009Article
- BH3-only proteins in rheumatoid arthritis: potential targets for therapeutic intervention.Oncogene · 2008Review
- Induction of tolerance to cardiac allografts using donor splenocytes engineered to display on their surface an exogenous fas ligand protein.Journal of immunology (Baltimore, Md. : 1950) · 2008Article
- Gene therapy for arthritis.Modern rheumatology · 2008Review
- Pro-apoptotic Bid is required for the resolution of the effector phase of inflammatory arthritis.Arthritis research & therapy · 2007Article
- Human immunodeficiency virus vector-mediated intra-articular expression of angiostatin inhibits progression of collagen-induced arthritis in mice.Rheumatology international · 2005Article
- Elimination of rheumatoid synovium in situ using a Fas ligand 'gene scalpel'.Arthritis research & therapy · 2005Article
- Gene therapy in animal models of rheumatoid arthritis: are we ready for the patients?Arthritis research & therapy · 2004Review
- The contralateral effect conferred by intra-articular adenovirus-mediated gene transfer of viral IL-10 is specific to the immunizing antigen.Gene therapy · 2003Article
- Gene therapy for arthritis.Gene therapy · 2003Review
- Gene therapy in nonhuman primate models of human autoimmune disease.Gene therapy · 2003Review
- Transgenic expression in mouse lung reveals distinct biological roles for the adenovirus type 5 E1A 243- and 289-amino-acid proteins.Journal of virology · 2002Article
- Endogenous regulation of a therapeutic transgene restores homeostasis in arthritic joints.The Journal of clinical investigation · 2002Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Both rheumatoid arthritis and animal models of autoimmune arthritis are characterized by hyperactivation of synovial cells and hyperplasia of the synovial membrane. The activated synovial cells produce inflammatory cytokines and degradative enzymes that lead to destruction of cartilage and bones. Effective treatment of arthritis may require elimination of most or all activated synovial cells. The death factor Fas/Apo-1 and its ligand (FasL) play pivotal roles in maintaining self-tolerance and immune privilege. Fas is expressed constitutively in most tissues, and is dramatically upregulated at the site of inflammation. In both rheumatoid arthritis and animal models of autoimmune arthritis, high levels of Fas are expressed on activated synovial cells and infiltrating leukocytes in the inflamed joints. Unlike Fas, however, the levels of FasL expressed in the arthritic joints are extremely low, and most activated synovial cells survive despite high levels of Fas expression. To upregulate FasL expression in the arthritic joints, we have generated a recombinant replication-defective adenovirus carrying FasL gene; injection of the FasL virus into inflamed joints conferred high levels of FasL expression, induced apoptosis of synovial cells, and ameliorated collagen-induced arthritis in DBA/1 mice. The Fas-ligand virus also inhibited production of interferon-gamma by collagen-specific T cells. Coadministration of Fas-immunoglobulin fusion protein with the Fas-ligand virus prevented these effects, demonstrating the specificity of the Fas-ligand virus. Thus, FasL gene transfer at the site of inflammation effectively ameliorates autoimmune disease.
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