Lower back pain
Peptide vaccines, based on the variable region gene elements of the b chain of the human T cell receptor of T cells found to be infiltrating human synovial tissue in RA, are currently being tested and look promising. lower back pain Tempromandibular joint arthritis case study. Other therapeutic approaches in which activated T cells are depleted have been less successful. For example, treatment of patients with a monoclonal antibody directed against CD4 successfully reduced the number of circulating CD4+ T cells, but did not induce a significant clinical response in patients with rheumatoid arthritis. (top of section) Targeting the propagation stage of disease Some approaches that are being studied or considered: Inhibit endothelial cell adhesion molecule expression This approach involves the administration of anti-ICAM, -ELAM, -VCAM, -VLA antibodies. lower back pain Synovial joints. The goal is to limit infiltration of synovium and synovial cavity by inflammatory cells. Clinical trials have been limited due to lack of humanized antibodies. Another approach is to inhibit angiogenesis in order to limit synovial hyperplasia. lower back pain Infoabdominal. Inhibition of cellular proliferation For example, with anti-PDGF or -FGF antibodies, or by the use of agents that promote apoptosis (e. g. , paclitaxel). The former presumes that there is enhanced cellular proliferation in rheumatoid synovium, but this remains doubtful. Inhibition of TNF-a and/or IL-1 Inhibition of TNF-a and IL-1 would be expected to reduce production of proteases, prostanoids, and other cytokines (IL-6, IL-8 and GM-CSF) in the rheumatoid joint and thereby reduce inflammation. There are several mechanisms by which TNF and IL-1 can be inhibited (slide). These include administration of: monoclonal antibodies directed against TNF or IL-1 (slide) antagonists of the TNF or IL-1 receptors (slide) soluble TNF or IL-1 receptors (slide) antiinflammatory cytokines (e. g. , IL-4 and IL-10) (slide). The first three approaches will theoretically block the interaction of a cytokine with its cognate membrane bound receptor, thereby preventing cell activation and release of inflammatory molecules The last approach seeks to counterbalance the proinflammatory effects of IL-1 and TNF. The most successful clinical responses to date, using cytokines or cytokine inhibitors in RA, have been with TNF inhibitors, namely a soluble TNF receptor and a humanized monoclonal antibody directed against TNF. These are discussed in detail elsewhere. (see Rheumatoid Arthritis and ACR Highlights) An initial trial with a soluble IL-1 receptor did not show efficacy but is likely to have targeted the wrong IL-1 receptor; studies are in progress currently with a recombinant form of the endogenous IL-1 receptor antagonist.
Lower back pain
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