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lüll The role of T-cell interleukin-17 in conducting destructive arthritis: lessons from animal models Lubberts E; Koenders MI; van den Berg WBArthritis Res Ther 2005[]; 7 (1): 29-37Interleukin-17 (IL-17) is a T cell cytokine spontaneously produced by cultures of rheumatoid arthritis (RA) synovial membranes. High levels have been detected in the synovial fluid of patients with RA. The trigger for IL-17 is not fully identified; however, IL-23 promotes the production of IL-17 and a strong correlation between IL-15 and IL-17 levels in synovial fluid has been observed. IL-17 is a potent inducer of various cytokines such as tumor necrosis factor (TNF)-alpha, IL-1, and receptor activator of NF-kappaB ligand (RANKL). Additive or even synergistic effects with IL-1 and TNF-alpha in inducing cytokine expression and joint damage have been shown in vitro and in vivo. This review describes the role of IL-17 in the pathogenesis of destructive arthritis with a major focus on studies in vivo in arthritis models. From these studies in vivo it can be concluded that IL-17 becomes significant when T cells are a major element of the arthritis process. Moreover, IL-17 has the capacity to induce joint destruction in an IL-1-independent manner and can bypass TNF-dependent arthritis. Anti-IL-17 cytokine therapy is of interest as an additional new anti-rheumatic strategy for RA, in particular in situations in which elevated IL-17 might attenuate the response to anti-TNF/anti-IL-1 therapy.|Animals[MESH]|Antirheumatic Agents/pharmacology/therapeutic use[MESH]|Arthritis, Experimental/drug therapy/pathology/*physiopathology[MESH]|Arthritis, Rheumatoid/drug therapy/*etiology/pathology/physiopathology[MESH]|Autoimmune Diseases/physiopathology[MESH]|Bone and Bones/pathology[MESH]|Carrier Proteins/physiology[MESH]|Cartilage, Articular/pathology[MESH]|Cytokines/biosynthesis/genetics[MESH]|Gene Expression Regulation/physiology[MESH]|Humans[MESH]|Inflammation/physiopathology[MESH]|Interleukin-17/antagonists & inhibitors/*physiology[MESH]|Interleukins/physiology[MESH]|Membrane Glycoproteins/physiology[MESH]|Mice[MESH]|Neutrophils/pathology[MESH]|Osteoclasts/pathology[MESH]|RANK Ligand[MESH]|Rats[MESH]|Receptor Activator of Nuclear Factor-kappa B[MESH]|Receptors, Interleukin-17[MESH]|Receptors, Interleukin/physiology[MESH]|Species Specificity[MESH]|Synovial Fluid/metabolism[MESH]|T-Lymphocytes/*metabolism[MESH]|Tumor Necrosis Factor-alpha/physiology[MESH] |