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滑膜成纤维细胞介导RA关节损伤的免疫学机制 被引量:3

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摘要 类风湿性关节炎(rheumatoid arthritis,RA)的关节破坏主要发生在血管翳增生浸润的软骨部位。滑膜组织血管翳可分为具免疫作用和侵蚀作用的两部分。前者由位于滑膜组织衬里下层的T细胞、B细胞、巨噬细胞和树突状细胞组成,介导抗原提呈、产生抗体和细胞因子,与滑膜炎症和过度增生有关;后者主要指紧邻骨和软骨损伤周围的滑膜组织和细胞,由过度增生的滑膜成纤维细胞(fibroblast-like synoviocyte,FLS)和血管翳共同组成。在RA的病理进展中,FLS发生活化并能产生大量炎症因子、基质蛋白和组织水解酶,造成局部炎症和关节软骨破坏,继而导致整个关节的损伤。本文就近年来的研究进展进行综述。
出处 《现代免疫学》 CAS CSCD 北大核心 2013年第6期518-521,共4页 Current Immunology
基金 973项目(2010CB529103)
关键词 RA FLS 关节损伤
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参考文献30

  • 1Neumann E,Le{vre S,Zimmermann g,et a[. Rheumatoid ar- thritis progression mediated by activated synovial {ibroblasts [J]. Trends Mol Med,2010,16:458-468.
  • 2Bartok B, Firestein GS. Fibroblast-like synoviocytes: key eb {ector cells in rheumatoid arthritis [J]. Immuno[ Rev, 2010, 233 : 233-255.
  • 3Cafxete JD,Celis R, Moll C,et ag. Clinical significance of syno- vial lymphoid neogenesis and its reversal after anti-tumour necrosis factor ct therapy in rheumatoid arthritis [J]. Ann Rheum Dis, 2009,68 = 751-756.
  • 4王险峰,陈森洲,侯巧燕.缺氧诱导因子-1α和血管内皮细胞生长因子在胶原性关节炎动物模型中的表达与意义[J].现代免疫学,2010,30(3):212-216. 被引量:9
  • 5Perlman H,Pope RM. The synovial lining micromass system toward rheumatoid arthritis in a dish [J]? Arthritis Rheum 2010,62:643-646.
  • 6Ekwall A-KH, Eisler T, Anderberg C, et al. The tumour-as- soeiated glycoprotein podoplanin is expressed in fibroblast-like synoviocytes of the hyperplastic synovial lining layer in rheu- matoid arthritis [J]. Arthritis Res Ther,2011,13 : 1-12.
  • 7Connor AM, Mahomed N, Gandhi R, et al. TNFa modulates protein degradation pathways in rheumatoid arthritis synovial fibroblasts [J]. Arthritis Res Ther,2012,14 1-19.
  • 8E1 Gendi SS,Moniem AE,Tawfik NM,et al. Value of serum and synovial fluid activin A and inhibin A in some rheumatic diseases [J]. Int J Rheum Dis,2010,13:273-279.
  • 9Sarkar S, Zhou X,Justa S,et al. Interleukin-22 reduces the se- verity of eo[lagen-ndueed arthritis in association with in- creased levels of interleukin-10 [J]. Arthritis Rheum, 2013, 65,960-971.
  • 10Lin J, Zhou Z, Huo R, et al. Cyr61 induces IL-6 production by fibroblast-like synoviocytes promoting Th17 differentiation in rheumatoid arthritis [J]. J Immunol, 2012,188 : 5776-5784.

二级参考文献10

  • 1Sivakumar B, Akhavani MA, Winlove CP, et al. Synovial hypoxia as a cause of tendon rupture in rheumatoid arthritis[J].J Hand Surg Am, 2008, 33: 49-58.
  • 2Baharav E, Mor F, Halpern M, etal. Lactobacillus GG bacteria ameliorate arthritis in Lewis rats[J].J Nutr, 2004, 134: 1964-1969.
  • 3Tsubaki T, Arita N, Kawakami T, etal. Characterization of histopathology and gene-expression profiles of synovitis in early rheumatoid arthritis using targeted biopsy specimens [J]. Arthritis Res Ther, 2005, 7: 825-836.
  • 4Rudolph EH, Woods JM. Chemokine expression and regulation of angiogenesis in rheumatoid arthritis[J]. Curr Pharm Des, 2005, 11:613-631.
  • 5Gaber T, Dziurla R, Tfipmacher R, et al. Hypoxia inducible factor HIF in rheumatology:low 02, See what HIF can do[J].Ann Rheum Dis, 2005, 64:971-980.
  • 6Tang N, WangL, Esko J, etal. Loss of HIF-1alpha in endothelial cells disrupts a hypoxia-driven VEGF autocrine loop necessary for tumorigenesis[J]. Cancer Cell, 2004, 6: 485- 495.
  • 7Peter CL, Morris CJ, Map PI, et al. The transcription factor hypoxia inducible factor 1 alpha and Ets-1 colocalize in the hypoxic synovium of inflamed joints in adjuvant-induced arthritis[J]. Arthritis Rheum, 2004, 50: 291-296.
  • 8Cramer T, Yamanichi Y, Clausen BE, et al. HIF-1alpha is essential for myeloid cell-mediated inflammation[J]. Cell, 2003,112:645-657.
  • 9Paleolog EM. The vasculature in rheumatoid arthritis: cause or consequence[J].Int J Exp Pathol, 2009,90:249-261.
  • 10韩晓枫,马宝骊,张继英,柏峻,王利,郝爱民.鸡胶原II型诱导大鼠类风关模型的建立[J].上海免疫学杂志,2001,21(6):330-333. 被引量:36

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