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Part of the book series: Progress in Inflammation Research ((PIR))

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Abstract

Interleukin-1 (IL-1) plays a central role in the pathophysiology of rheumatoid arthritis (RA) [1]. The IL-1 gene family includes IL-1α, IL-lβ and IL-1 receptor antagonist (IL-IRa) [2], Extracellular IL-lα, which is membrane-associated, and IL- lβ, which is the soluble form, are agonist molecules that can influence the functions of most cell types. Activated monocytes and macrophages are the principal source of IL-la and IL-lβ. There are two distinct IL-1 receptors, designated type I (IL-1RI) and type II (IL-1RII) [3, 4]. IL-1 binding to IL-1RI results in signal transduction and cell activation. IL-1RII is a “decoy” receptor that functions by scavenging IL-la and IL-lβ, but does not have a role in cell signaling [5]. Soluble IL-1RII (sIL-lRII) is important in regulating IL-l-mediated functions. Binding of IL-1 to IL-1RI produces many effects that are central to the pathogenesis of RA [3, 4, 68]. The pivotal role of IL-1 in the pathophysiology of RA was highlighted by inducing the pathologic features of RA in rabbits following transfer of the human IL-lβ gene, resulting in the constitutive expression of IL-lβ by synovial cells [9].

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© 2005 Birkhäuser Verlag Basel/Switzerland

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Bresnihan, B. (2005). Anakinra in rheumatoid arthritis. In: Day, R.O., Fürst, D.E., van Riel, P.L.C.M., Bresnihan, B. (eds) Antirheumatic Therapy: Actions and Outcomes. Progress in Inflammation Research. Birkhäuser Basel. https://doi.org/10.1007/978-3-7643-7726-7_15

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  • DOI: https://doi.org/10.1007/978-3-7643-7726-7_15

  • Publisher Name: Birkhäuser Basel

  • Print ISBN: 978-3-7643-6595-0

  • Online ISBN: 978-3-7643-7726-7

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