Abstract
This is a review concerning the role of interleukin-17, a proinflammatory cytokine, produced by activated memory CD4+ T cells, in pathogenesis of rheumatoid arthritis. As interleukin-17 shares properties with IL-1 and TNF-alpha, it may induce joint inflammation and bone and cartilage destruction. This cytokine is found in synovial fluids of patients with rheumatoid arthritis, and produced by rheumatoid arthritis synovium. It increases IL-6 production, induces collagen degradation and decreases collagen synthesis by synovium and cartilage and proteoglycan synthesis in cartilage. Interleukin-17 is also able to increase bone destruction and reduce its formation. Blocking of interleukin-17 with specific inhibitors provides a protective inhibition of cartilage and bone degradation.
Publication types
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Comparative Study
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English Abstract
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Review
MeSH terms
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Animals
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Arthritis, Rheumatoid / etiology*
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Arthritis, Rheumatoid / pathology
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Arthritis, Rheumatoid / physiopathology
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Cartilage, Articular / metabolism
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Cartilage, Articular / pathology
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Cells, Cultured
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Collagen / biosynthesis
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Collagen / metabolism
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Gene Expression
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Humans
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Interleukin-1 / physiology
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Interleukin-17 / analysis
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Interleukin-17 / antagonists & inhibitors
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Interleukin-17 / biosynthesis
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Interleukin-17 / genetics
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Interleukin-17 / physiology*
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Mice
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Osteoblasts / cytology
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Osteoblasts / pathology
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Proteoglycans / metabolism
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Synovial Fluid / chemistry
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Synovial Membrane / metabolism
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Tumor Necrosis Factor-alpha / physiology
Substances
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Interleukin-1
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Interleukin-17
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Proteoglycans
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Tumor Necrosis Factor-alpha
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Collagen