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课件:脊柱关节炎早期诊断新进展.ppt
欢迎索阅并积极参与讨论、竟猜 谢谢! THANK YOU SUCCESS * * 可编辑 * Figure 2:MRI demonstrating acute inflammation highly suggestive of sacroiliitis associated with spondyloarthropathy in a 12-year-old HLA-B27-positive male. The patient presented with right-hip pain, and on physical examination exhibited a decreased range of motion and tenderness to palpation of the right sacroiliac joint. Radiographs were normal at presentation, but the MRI revealed asymmetric high signal in the right sacroiliac joint suggestive of sacroiliitis. The patient responded well to treatment with NSAIDs initially, but required a corticosteroid hip injection approximately 2 years later. At that time, radiographs revealed slight sclerosis of the right sacroiliac joint with normal hip-joint spaces and no definite bony erosions. The author thanks Drs egla Rabinovich (Duke University, Durham, NC, USA) and edward Fels (Rheumatology Associates, Portland, Me, USA) for providing the image. * Figure 3: Hypothetical functional interactions between gene products associated with ankylosing spondylitis. The genes HLA-B27, ERAP1, IL23R, IL1R2, TRADD, TNFR1, CARD9, and ANTXR2 (not shown) have definite or suggested associations with AS. One mechanism linking HLA-B27 to the IL-23/IL-17 (TH17) axis involves misfolding and UPR activation triggered by MHC class I upregulation. UPR activation enhances production of IL-23 and IFN-β in response to certain PRR agonists. CARD9 mediates IL-23 induction in response to fungal cell wall components through the PRR, Dectin-1. ERAP1 influences the quality and/or quantity of peptides available for MHC class I molecules, and might impact not only cell-surface complexes, but also the folding efficiency of HLA-B27. ERAP1 (also known as ARTS1) is also an aminopeptidase regulator of TNF (TNFR1) receptor shedding, and also influences IL-6 and IL-1R2 (IL1R2) receptors. Polymorphisms in TNFR1 and TRADD, a mediator of TNF signaling, could influence downstream effects perhaps contributing to phenoty
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