Abstract
Rheumatoid arthritis (RA) is a chronic, inflammatory joint disease with systemic involvement that affects about 1% of the Western population. The progressive destruction of affected joints is a major characteristic of the disease and distinguishes RA from other acute and chronic arthritides. The etiology of RA is unknown, and a variety of genetic and environmental factors are being discussed as potential causes of the disease. However, in contrast to our incomplete understanding of the etiology, the knowledge about molecular mechanisms leading to joint destruction has advanced considerably over the past years. Thus, a large number of studies have investigated the presence and interplay of several types of cells in rheumatoid synovium, such as lymphocytes, macrophages and fibroblasts. They have led to the understanding that cells in the rheumatoid synovium form a network, which interacts through direct cell-to cell contacts as well as the release of a multitude of cytokines. The use of novel molecular techniques together with the development of new animal models has revised our concept on the pathogenesis of RA and specifically on the role of fibroblasts in initiation and progression of joint destruction. This article will review current data and hypotheses on disease mechanisms by which fibroblasts are involved in the destruction of joints in RA.
Keywords: inflammation, synovial hyperplasia, lymphocytes, major histocompatibility complex, osteoarthritis, transcription factors, matrix degrading enzymes, collagenases
Current Pharmaceutical Design
Title: The Role of Synovial Fibroblasts in Mediating Joint Destruction in Rheumatoid Arthritis
Volume: 11 Issue: 5
Author(s): Ingmar Meinecke, Edita Rutkauskaite, Steffen Gay and Thomas Pap
Affiliation:
Keywords: inflammation, synovial hyperplasia, lymphocytes, major histocompatibility complex, osteoarthritis, transcription factors, matrix degrading enzymes, collagenases
Abstract: Rheumatoid arthritis (RA) is a chronic, inflammatory joint disease with systemic involvement that affects about 1% of the Western population. The progressive destruction of affected joints is a major characteristic of the disease and distinguishes RA from other acute and chronic arthritides. The etiology of RA is unknown, and a variety of genetic and environmental factors are being discussed as potential causes of the disease. However, in contrast to our incomplete understanding of the etiology, the knowledge about molecular mechanisms leading to joint destruction has advanced considerably over the past years. Thus, a large number of studies have investigated the presence and interplay of several types of cells in rheumatoid synovium, such as lymphocytes, macrophages and fibroblasts. They have led to the understanding that cells in the rheumatoid synovium form a network, which interacts through direct cell-to cell contacts as well as the release of a multitude of cytokines. The use of novel molecular techniques together with the development of new animal models has revised our concept on the pathogenesis of RA and specifically on the role of fibroblasts in initiation and progression of joint destruction. This article will review current data and hypotheses on disease mechanisms by which fibroblasts are involved in the destruction of joints in RA.
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Cite this article as:
Meinecke Ingmar, Rutkauskaite Edita, Gay Steffen and Pap Thomas, The Role of Synovial Fibroblasts in Mediating Joint Destruction in Rheumatoid Arthritis, Current Pharmaceutical Design 2005; 11 (5) . https://dx.doi.org/10.2174/1381612053381945
DOI https://dx.doi.org/10.2174/1381612053381945 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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