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  Indian J Med Microbiol
 

Figure 1: Pathology of rheumatoid arthritis. Rheumatoid arthritis is an autoimmune systemic disease mediated by T-cells and B-cells. T-cell creates interleukin-17 which can stimulate macrophages to produce inflammatory cytokines, including interleukin-1, interleukin-6, and tumor necrosis factor-α. T-cell also expresses receptor activator of nuclear factor-kappa B ligand, which together with inflammatory cytokines activates the osteoclast leading to bone erosion. Inflammatory cytokines activate synovial cells to produce protease, which can cause cartilage degradation. Rheumatoid factor and anti-citrullinated protein antibodies are the two most important autoantibodies usually produced by plasma cells. All of these play an important role in the pathogenesis of rheumatoid arthritis

Figure 1: Pathology of rheumatoid arthritis. Rheumatoid arthritis is an autoimmune systemic disease mediated by T-cells and B-cells. T-cell creates interleukin-17 which can stimulate macrophages to produce inflammatory cytokines, including interleukin-1, interleukin-6, and <i>tumor necrosis factor</i>-α. T-cell also expresses receptor activator of nuclear factor-kappa B ligand, which together with inflammatory cytokines activates the osteoclast leading to bone erosion. Inflammatory cytokines activate synovial cells to produce protease, which can cause cartilage degradation. Rheumatoid factor and anti-citrullinated protein antibodies are the two most important autoantibodies usually produced by plasma cells. All of these play an important role in the pathogenesis of rheumatoid arthritis