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IL-18 is produced by articular chondrocytes and induces proinflammatory and catabolic responses

Academic Article
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Overview

authors

  • Olee, T.
  • Hashimoto, S.
  • Quach, J.
  • Lotz, Martin

publication date

  • January 1999

journal

  • Journal of Immunology  Journal

abstract

  • IL-18, a cytokine originally identified as IFN-gamma-inducing factor, is a member of the IL-1 family of proteins. Because IL-1alpha and IL-1beta are important mediators in the pathogenesis of arthritis, the present study addresses the expression of IL-18 and its role in regulating in articular chondrocytes. IL-18 mRNA was induced by IL-1beta in chondrocytes. Chondrocytes produced the IL-18 precursor and in response to IL-1 stimulation secreted the mature form of IL-18. Studies on IL-18 effects on chondrocytes showed that it inhibits TGF-beta-induced proliferation and enhances nitric oxide production. IL-18 stimulated the expression of several genes in normal human articular chondrocytes including inducible nitric oxide synthase, inducible cyclooxygenase, IL-6, and stromelysin. Gene expression was associated with the synthesis of the corresponding proteins. Treatment of normal human articular cartilage with IL-18 increased the release of glycosaminoglycans. These finding identify IL-18 as a cytokine that regulates chondrocyte responses and contributes to cartilage degradation.

subject areas

  • Arthritis
  • Cartilage, Articular
  • Cell Division
  • Chondrocytes
  • Gene Expression Regulation
  • Growth Inhibitors
  • Humans
  • Interleukin-18
  • Knee Joint
  • Nitric Oxide
  • Protein Biosynthesis
  • Proteoglycans
  • RNA, Messenger
  • Recombinant Proteins
  • Transforming Growth Factor beta
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Identity

International Standard Serial Number (ISSN)

  • 0022-1767

PubMed ID

  • 9916738
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Additional Document Info

start page

  • 1096

end page

  • 1100

volume

  • 162

issue

  • 2

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