Rheumatoid arthritis is an autoimmune disease that causes chronic inflammation of the joints which eventually leads to their destruction. In rheumatoid arthritis affected joints, lymphocytes are activated causing cytokines, such as tumor necrosis factor (TNF) and interleukin-1 (IL-1), to be expressed in the inflamed areas. T cells from Rheumatoid arthritis patients recognize cartilage protein and a protein encoded by the bacterium that causes tuberculosis, thus suggesting that mycobacterial infection may trigger Rheumatoid arthritis. The incidence of Rheumatoid arthritis has a negative correlation with thymus function. Patients with Rheumatoid arthritis inevitably experience pain alongside the swelling and tenderness associated with rheumatoid joint inflammation. IL-1 and TNF strongly induce the production of PGE2, leukotrienes and platelet-activating factor, which are involved in the pain mechanism. Tumor necrosis factor (TNF) is a cytokine produced by macrophages that causes the inflammation associated with Rheumatoid arthritis. Medications currently available to combat Rheumatoid arthritis function by binding TNF and preventing it from functioning.
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