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Interleukin-1 and tumor necrosis factor: Rheumatoid arthritis and pain

  • Chapter
Cytokines and Pain

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

Abstract

Rheumatoid arthritis (RA) is a chronic inflammatory disorder of unknown etiology. It is a common disease, with a prevalence of 1 to 2% in the United States. Women are more commonly affected than men (average ratio is 3:1), and the disease produces substantial morbidity as well as an increase in mortality [1]. Although the etiology of RA is unknown, it is generally agreed that it represents an autoimmune disease that involves both the humoral and cellular arms of the immune response. A complex interaction of genetic, immunological, and local factors has been invoked to account for the differing patterns of joint involvement and progression of disease. Certainly RA may be caused by inflammatory CD4 T cells specific for a joint antigen which triggers the release of cytokines (and other mediators) that initiate local inflammation within the joint. This causes swelling, accumulation of polymorphonuclear leukocytes and macrophages, and damage to cartilage, leading to the destruction of the joint. Laboratory and clinical evidence suggests that proinflammatory cytokines, particularly interleukin-1 (IL-1) and tumor necrosis factor (TNF), have an important role in the pathogenesis of RA [2].

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  1. Department of Pharmacology, Amgen Inc., One Amgen Center Drive, Thousand Oaks, CA, 91320, USA

    David Martin

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  1. Dept. of Psychology, University of Colorado at Boulder, Boulder, CO, 80309-0345, USA

    Linda R. Watkins  & Steven F. Maier  & 

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Martin, D. (1999). Interleukin-1 and tumor necrosis factor: Rheumatoid arthritis and pain. In: Watkins, L.R., Maier, S.F. (eds) Cytokines and Pain. Progress in Inflammation Research. Birkhäuser, Basel. https://doi.org/10.1007/978-3-0348-8749-6_9

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  • DOI: https://doi.org/10.1007/978-3-0348-8749-6_9

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