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group_2_presentation_2_-_juvenile_arthritis [2017/03/08 16:46]
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group_2_presentation_2_-_juvenile_arthritis [2018/01/25 15:18] (current)
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 Cytokines are protein messengers that transmit signals from one cell to another by binding to specific receptors on the surface of cells. Both pro- and anti-inflammatory cytokines, chemokines, and mitogenic factors are produced, but proinflammatory mediators predominate during the active phase of disease.Tumor necrosis factor alpha (TNFα)‎, IL-1, IL-6 and IL-17 are of key importance in the pathogenesis of inflammation in RA. IL-1 and TNFα‎ are also key players in the regulation of mediators of connective tissue damage by synoviocytes,​ including matrix metalloproteinases (MMPs) and prostaglandins (Nath Maini, 2010). Cytokines are protein messengers that transmit signals from one cell to another by binding to specific receptors on the surface of cells. Both pro- and anti-inflammatory cytokines, chemokines, and mitogenic factors are produced, but proinflammatory mediators predominate during the active phase of disease.Tumor necrosis factor alpha (TNFα)‎, IL-1, IL-6 and IL-17 are of key importance in the pathogenesis of inflammation in RA. IL-1 and TNFα‎ are also key players in the regulation of mediators of connective tissue damage by synoviocytes,​ including matrix metalloproteinases (MMPs) and prostaglandins (Nath Maini, 2010).
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 +<box 60% round right |>​{{:​p4.png|}}</​box|Figure 8: Summary of the pathogenic pathways in JIA. Retrived from: https://​www.researchgate.net/​profile/​Abdullah_Nahian/​publication/​263585727/​figure/​fig1/​AS:​202832654409738@1425370481906/​Figure-illustrates-the-pathogenic-pathways-of-rheumatoid-arthritis-following-31-38.png>​
  
 ACPAs may also bind to citrullinated proteins directly in the synovial membrane. Immune complexes between citrullinated proteins ,such as fibrinogen, and ACPA-igG can drive inflammation (including the production of IL-6 and tumor necrosis factor) by engaging both toll-like receptor (TLR4) and Fc receptors (Nath Maini, 2010). ACPAs may also bind to citrullinated proteins directly in the synovial membrane. Immune complexes between citrullinated proteins ,such as fibrinogen, and ACPA-igG can drive inflammation (including the production of IL-6 and tumor necrosis factor) by engaging both toll-like receptor (TLR4) and Fc receptors (Nath Maini, 2010).
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 Both ACPA- and RF-dependent events could contribute to the initiation and propagation of chronic synovial inflammation,​ and further synergize with T cell activation and enhance the local production of autoantibodies (McInnes & Schett, 2011). Both ACPA- and RF-dependent events could contribute to the initiation and propagation of chronic synovial inflammation,​ and further synergize with T cell activation and enhance the local production of autoantibodies (McInnes & Schett, 2011).
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-<box 60% round right |>​{{:​p4.png|}}</​box|Figure 8: Summary of the pathogenic pathways in JIA. Retrived from: https://​www.researchgate.net/​profile/​Abdullah_Nahian/​publication/​263585727/​figure/​fig1/​AS:​202832654409738@1425370481906/​Figure-illustrates-the-pathogenic-pathways-of-rheumatoid-arthritis-following-31-38.png>​ 
  
 ===Bone Destruction=== ===Bone Destruction===
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