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Modulation of the IκB Kinase/Nuclear Factor-κB Pathway by Gene Therapy

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Modern Therapeutics in Rheumatic Diseases
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Abstract

In rheumatoid arthritis (RA), the synovium is hypertrophic and edematous, and villous projections of synovial tissue protrude into the joint cavity. Cartilage degradation primarily results from the action of extracellular proteolytic enzymes produced in the local microenvironment at the invasive front of the synovial tissue (pannus). Although the etiology of RA remains elusive, immune-mediated mechanisms are of crucial importance. It has become clear that macrophages and fibroblast-like synoviocytes play a critical role as effector cells in chronic synovial inflammation (1–3). T cells could contribute to the excessive production of proinflammatory cytokines by stimulation of these effector cells (4–6). Both macrophages and fibroblast-like synoviocytes are highly activated and secrete a variety of cytokines as well as matrix metalloproteinases.

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© 2002 Humana Press, Inc., Totowa, NJ

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Tak, P.P., Firestein, G.S. (2002). Modulation of the IκB Kinase/Nuclear Factor-κB Pathway by Gene Therapy. In: Tsokos, G.C. (eds) Modern Therapeutics in Rheumatic Diseases. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-59259-239-5_35

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  • DOI: https://doi.org/10.1007/978-1-59259-239-5_35

  • Publisher Name: Humana Press, Totowa, NJ

  • Print ISBN: 978-1-4684-9708-3

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