The NF-kB Pathway as a Potential Target for Autoimmune Disease Therapy

Authors: Bacher, Susanne1; Schmitz, M. L.1

Source: Current Pharmaceutical Design, Volume 10, Number 23, September 2004 , pp. 2827-2837(11)

Publisher: Bentham Science Publishers

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Abstract:

A battery of proinflammatory agents triggers the activation of NF-kgrB. This inducible transcription factor participates in the expression of an exceptionally large number of target genes, many of them contributing to the regulation of innate and adaptive immunity. Since some target genes also function as NF-kgrB activators, activation of this transcription factor allows the establishment of a signal amplification loop. Dysregulation of the NF-kgrB system and hyperactivated expression of inflammatory mediators are often found in association with some autoimmune diseases, which occur upon mounting of the adaptive immune response against self-antigens. In this review we summarize the relevance of aberrant NF-kgrB signaling for the development and perpetuation of some autoimmune diseases such as rheumatoid arthritis, diabetes mellitus type 1 and Crohn's disease. The assets and drawbacks of systemic or cell-type specific NF-kB inhibitors and their potential use in therapy of autoimmune diseases are critically discussed.

Keywords: ikk; autoimmune disease; inflammation; crohns disease; rheumatoid arthritis

Document Type: Review article

DOI: 10.2174/1381612043383584

Affiliations: 1: University of Bern, Department of Chemistry and Biochemistry, Freiestr. 3, CH-3012 Bern (Switzerland)

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