• Presse Med · Mar 2000

    Review

    [Role of anti-TNF therapy in rheumatoid arthritis].

    • O Meyer.
    • Service de Rhumatologie, Hôpital Bichat, Paris. olivier.meyer@bch.ap-hop-paris.fr
    • Presse Med. 2000 Mar 11; 29 (9): 463-8.

    AbstractTUMOR NECROSIS FACTOR: TNF is a cytokine produced by several types of cells, but mainly by monocyte-macrophages, activated endothelial cells, fibroblasts, and joint cartilage chondrocytes. The circulating form of TNF alpha (homotrimere) is derived from its membrane form by cleavage induced by a metalloprotease called TACE. This cytokine plays a pivotal role in the inflammatory reaction in conjunction with IL-1 and IL-6. The effect of TNF alpha is mediated by two membrane receptors carried on the surface of target cells (TNF-RI p55 and TNF-RII p75) which are released into the biological fluids (synovial fluid and plasma). ARGUMENTS FOR A PATHOGENIC ROLE: Transgenic mice carrying the human gene for TNF alpha develop polyarthritis suggesting this cytokine is directly implicated in the pathogenesis. In diverse cell types in rheumatoid joints, TNF alpha and its receptors can be identified by immunohistochemistry techniques as can TNF alpha mRNA by RT-PCR.

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