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类风湿关节炎大鼠血清Th1/Th2水平及意义 被引量：7

The level and the significance of Th1/Th2 in serum of rats with rheumatoid arthritis
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摘要 目的:初步探讨类风湿关节炎大鼠免疫功能紊乱的机制。方法:采用酶联免疫吸附法(ELISA)检测类风湿关节炎大鼠血清中Th1细胞分泌的细胞因子IFN-γ和Th2细胞分泌的细胞因子IL-4的水平。结果:类风湿关节炎大鼠血清中IFN-γ的水平与正常组相比明显升高(p<0.01),IL-4的水平明显降低(p<0.01)。结论:在类风湿关节炎大鼠血清中Th1/Th2细胞分泌的细胞因子水平存在着明显失衡,两者以Th1细胞分泌细胞因子占优势,这可能与其发病机制密切相关。 Objective：To research the mechanisms of immune function disorder in the rats with rheumatoid arthritis（RA） . Methods：We used enzyme linked immunosorbent assay（ELISA） to detect the cytokines level of Th1 cell including interferon-gamma（IFN-γ） and those of Th2 cell including interleukine 4（IL-4） . These samples are serum of rats with RA respectively. Results：Comparing with the health groups,the level of IFN-γ in serum of rats with RA is obviously increased（p0.01） and the level of IL-4 is obviously decreased（p0.01） . Conclusion：There is obviously imbalance in Th1/Th2 cytokines level of serum of rats with RA. The cytokines level of Th1 cell predominate,it suggests which probably associate with the mechanism of RA.
作者 王娟 刘瑞洪 肖红波 毕慧欣 李智
机构地区 中南大学湘雅二医院肾内科 中南大学湘雅二医院老年科 国防科技大学医院内一科
出处 《现代生物医学进展》 CAS 2010年第2期246-247,共2页 Progress in Modern Biomedicine
关键词 类风湿关节炎 TH1/TH2细胞 IFN-Γ IL-4 Rheumatoid arthritis Th1/Th2 cell IFN-γ IL-4
分类号 R593.22 [医药卫生—内科学]
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参考文献10

  • 1冷建杭,蒋群芳,姜晓虹,卓广超,王克义,汪子伟.类风湿关节炎血清和滑液Th1/Th2细胞因子的水平及意义[J].浙江临床医学,2004,6(6):457-458. 被引量：6
  • 2邓安梅,仲人前,陈孙孝,施笑梅,孔宪涛.关节炎中B7:CD28CTLA-4共刺激途径的实验研究[J].中国免疫学杂志,2000,16(8):412-414. 被引量：42
  • 3Santana MA, Rosenstein Y. What it takes to become an effector T cell: the process, the cells involved, and the mechanisms [J]. J Cell Physiol, 2006,195(3):392-401.
  • 4Elewaut D,Keyser FD, Wever ND, et al. A comparative phenotypical analysis of rheumatoid nodules and rheumatoid synovium with special reference to adhesion molecules and activation markers [J]. Ann Rheum Dis, 2002, 57(8): 480-486.
  • 5Kanik K S, Hagiwara E, Yarboro CH, et al. Distinct patterns of cytokine secretion characterize new onset synovitis versus chronic rheumatoid arthritis [J]. J Rheumatol, 2002, 25(1): 16-22.
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  • 8Joosten LAB, Lubberts E Role ofIL 4 and IL 10 in murine collgen induced arthritis: protective effect of IL-4 and IL-10 treatment cartilage destruction [J]. Arthritis Rheum, 2003, 40:249-260.
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二级参考文献9

  • 1[1]Santana MA, Rosenstein Y. What it takes to become an effector T cell:the process, the cells involved, and the mechanisms. J Cell Physiol,2003,195(3) :392 ～ 401.
  • 2[2]Elewaut D, Keyser FD, Wever ND, et al. A comparative phenotypical analysis of rheumatoid nodules and rheumatoid synovium with special reference to adhesion molecules and activation markers. Ann Rheum Dis,1998,57(8) :480 ～ 486.
  • 3[3]Kanik KS, Hagiwara E, Yarboro CH, et al. Distinct patterns of cytokine secretion characterize new onset synovitis versus chronic rheumatoid arthritis. J Rheumatol, 1998, 25(1): 16～ 22.
  • 4[4]Racke MK, Bonomo A. Cytokine - induced immune deviation as a therapy for inflammatory autoimmune disease. J Exp Med, 1994, 180(8): 1961 ～ 1966.
  • 5[5]Simon AK, Seipelt E, Seiper J. Divergent T- cell Cytokine patterns in inflammatory arthritis. Proc Natl Acad Sci USA, 1994, 91(7):8562～8566.
  • 6[6]Paludan SR. Interleukin - 4 and interferon - gamma: the quintessence of a mutual antagonistic relationship. Scand J Immunol, 1998, 48(5):459 ～ 468.
  • 7[7]Whalen JD, Lechman EL, Carlos CA, aeyet al. Adenoviral tranfer of the viral IL- 10 gene periarticularly to mouse paws suppresses development of collagen - induced arthritis in both injected and uninjected paws. J Immunol, 1999,162(6) :3625 ～ 3632.
  • 8[8]Joosten LA, Lubberts E, Durez P, et al. Role of interleukin - 4 and interleukin - 10 in murine collagen-induced arthritis: protective effect of interleukin - 4 and interleukin - 10 treatment on cartilage destruction.Arthritis Rheum, 1997,40(2) :249 ～ 260.
  • 9Ranjeny Thomas. Antigen-presenting cells in rheumatoid arthritis[J] 1998,Springer Seminars in Immunopathology(1-2):53～72

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现代生物医学进展
2010年 第2期

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