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Interleukin-6--a key mediator of systemic and local symptoms in rheumatoid arthritis Cronstein BNBull NYU Hosp Jt Dis 2007[]; 65 Suppl 1 (�): S11-5Interleukin-6 (IL-6) is a pleiotropic cytokine, present at elevated levels in patients with rheumatoid arthritis (RA). Il-6 signaling involves both a specific IL-6 receptor (IL-6R) and a ubiquitous signal-transducing protein, gp130 that is also utilized by other members of the IL-6 family. Il-6 signaling occurs by two mechanisms. Conventional signaling involves the binding of IL-6 to transmembrane IL-6R on cells expressing this receptor. In contrast, trans-signaling involves binding between the complex of soluble IL-6R/IL-6 and membrane-bound gp130. Trans-signaling allows IL-6 to affect cells that do not express IL-6R, including many synovial cells. The biological activities of IL-6 contribute to both systemic and local RA symptoms. Il-6 is a strong inducer of the acute-phase response, which can result in fever, secondary amyloidosis, anemia, and elevations in acute-phase proteins, such as C-reactive protein (CRP). The ability of IL-6 to induce B-cell differentiation may lead to the formation of rheumatoid factor and other autoantibodies. In joints, IL-6 promotes osteoclast activation and induces the release of matrix metalloproteinases, thus contributing to joint damage. In patients with RA, IL-6 levels correlate with markers of disease activity and clinical symptoms, and animal studies support the concept that this cytokine plays a role in the development of inflammatory arthritis. Clinical trials with tocilizumab, a humanized monoclonal antibody to soluble IL-6R, have shown that blocking IL-6 signaling reduces RA symptoms and markers of disease activity. Current evidence thus strongly supports the association between IL-6 and RA symptoms and suggests that IL-6 blockade will be a useful therapeutic strategy for patients with this disease.|Animals[MESH]|Antibodies, Monoclonal, Humanized[MESH]|Antibodies, Monoclonal/therapeutic use[MESH]|Antirheumatic Agents/therapeutic use[MESH]|Arthritis, Rheumatoid/drug therapy/*physiopathology[MESH]|Cytokine Receptor gp130/physiology[MESH]|Humans[MESH]|Interleukin-6/immunology/*physiology[MESH]|Receptors, Interleukin-6/immunology/physiology[MESH]|Signal Transduction[MESH] |