Corpus ID: 45400869

Lessons from animal models of arthritis.

@article{Berg2002LessonsFA,
  title={Lessons from animal models of arthritis.},
  author={W. B. van den Berg},
  journal={Current rheumatology reports},
  year={2002},
  volume={4 3},
  pages={
          232-9
        }
}
There is increasing thought that autoantibodies to systemic self-antigens may provide a principal effector mechanism for the initiation and propagation of joint inflammation. The recent identification of arthritis transfer with antibodies to the self-antigen glucose-6-phosphate isomerase has boosted this interest. Fc receptor involvement in arthritis has been evaluated, identifying pro-inflammatory and inhibitory Fc gamma receptor subtypes, and demonstrating a link between Fc gamma receptor… Expand
Is there a rationale for combined TNF and IL-1 blocking in arthritis?
TLDR
If elements of the models apply to the arthritic process in RA patients, it is necessary to block IL-1 in addition to TNF, which is a major inflammatory mediator in RA and a potent inducer ofIL-1. Expand
IL-18 in autoimmunity: review.
TLDR
It is proposed that the disturbed mechanism of innate immunity, resulting from macrophage activation through innate immunity receptors (TLR/IL-1R family), may be the basis of pathologically high levels of IL-18 production and activation. Expand
Treatment of arthritis with a selective inhibitor of c-Fos/activator protein-1
TLDR
Selective inhibition of c-Fos/AP-1 resolves arthritis in a preclinical model of the disease. Expand
Pathogenesis of rheumatoid arthritis and c-Fos/AP-1
TLDR
The blockade of IL-1β and/or c-Fos/AP-1 can be promising as an effective therapy for rheumatoid joint destruction in addition to the currently available TNFα blocking agents that act mainly on arthritis. Expand
Cytokines and Joint Injury
TLDR
The role of tumour necrosis factor in rheumatoid arthritis, the role of IL-1 and IL-18 in inflammation, and the importance to cytokine regulation in tissue destruction and repair are studied. Expand
Interleukin-18: a therapeutic target in rheumatoid arthritis?
TLDR
The biology of, and experimental approaches to IL-18 neutralisation are reviewed, together with speculation as to the relative merits of IL- 18 as an alternative to existing targets are speculated. Expand
The Inhibitory Co-Receptor, PECAM-1 Provides a Protective Effect in Suppression of Collagen-Induced Arthritis
TLDR
Observations suggest that PECAM-1 plays a crucial role in the suppression of development of autoimmune arthritis in mouse models of collagen-induced arthritis and K/BxN passive transfer model that resembles many of the features of human rheumatoid arthritis. Expand
Pathogenesis of bone and cartilage destruction in rheumatoid arthritis.
TLDR
Enhanced understanding of the mechanisms underlying the processes of joint destruction will allow more selective and specific application of therapeutic agents that target these proinflammatory cytokines and, thus, more effective management of patients with RA and other inflammatory disorders. Expand
IL‐1β, IL‐6, KC and MCP‐1 are elevated in synovial fluid from haemophilic mice with experimentally induced haemarthrosis
TLDR
It is demonstrated, for the first time, that bleeding in knee joints of haemophilia A mice resulted in correlated increased levels of the pro‐inflammatory cytokines: IL‐1β, IL‐6, KC and the MCP‐1 in synovial fluid, which might contribute to further progression of the inflammatory process. Expand
Pathogenesis of Joint Destruction in Rheumatoid Arthritis
TLDR
Blockade of IL-1β and c-Fos/AP-1 influence each other’s gene expression and activity, resulting in an orchestrated cross-talk that is crucial to arthritic joint destruction, and thus, blockade of IL/Cfos/ap-1 can be most promising as a therapeutic target. Expand
...
1
2
3
4
...