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系统性红斑狼疮患者血浆白细胞介素-17A的表达及临床意义

Expression and clinical significance of plasma interleukin-17A in systemic lupus erythematosus
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摘要 目的:探讨白细胞介素-17A(IL-17A)在系统性红斑狼疮(SLE)患者血浆中的水平变化及其临床意义。方法:应用ELISA法检测初发SLE患者未用激素治疗组13例、激素治疗组47例及29名健康志愿者(对照组)血浆中IL-17A的水平,比较3组的差异并分析IL-17A水平与临床指标的关系。结果:未用激素治疗组IL-17A水平均高于对照组及激素治疗组(P<0.05和P<0.01)。IL-17A水平与红细胞沉降率和C4均呈负相关关系(P<0.05);而与C3、IgG、抗ds-DNA、SLE疾病活动性指数和24 h尿蛋白定量均无相关关系(P>0.05)。结论:未用激素治疗组血浆IL-17A的水平比对照组升高,IL-17A在SLE的发病中可能发挥着重要的作用,激素治疗可显著降低SLE患者IL-17A水平。 Objective:To investigate the changes of plasma interleukin-17A(IL-17A) level in patients with systemic lupus erythematosus(SLE) and analyze the clinical implication. Methods:Plasma IL-17A level was measured by ELISA from 60 SLE patients(13 without glucocorticoid treatment and 47 with glucocorticoid treatment) and 29 healthy persons.The relationship between IL-17A and clinical or laboratory parameters of SLE patients was explored. Results:IL-17A levels were elevated significantly in SLE patients without glucocorticoid treatment than in SLE patients with glucocorticoid treatment or healthy persons(P0.05-P0.01).The negative correlation was observed between IL-17A expression and C4,erythrocyte sedimentation rate(P0.05),but no correlation with C3,IgG,anti ds-DNA antibody,SLE disease activity index score and 24 h urine protein excretion(P0.05). Conclusions:The level of plasma IL-17A in SLE patient without glucocorticoid treatment was higher than in normal control.IL-17A might play an important role in the pathogenesis of SLE.Treatment with glucocorticoid can decrease IL-17A level in SLE significantly.
出处 《蚌埠医学院学报》 CAS 2012年第11期1287-1288,1293,共3页 Journal of Bengbu Medical College
基金 蚌埠医学院科研基金资助项目(BY0934)
关键词 系统性红斑狼疮 白细胞介素-17A 酶联免疫吸附试验 systemic lupus erythematosus interleukin-17A enzyme linked immunosorbent assay
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参考文献13

  • 1Jacob N, Stohl W. Cytokine disturbances in systemic lupus erythematosus [ J ]. Arthritis Res Ther,2011,13 (4) :228.
  • 2Kurasawa K, Hirose K, Sano H, et al. Increased interleukin-17 production in patients with systemic sclerosis [ J ]. Arthritis Rheum,2000,43 ( 11 ) :2455 - 2463.
  • 3Sarkar S, Fox DA. Targeting IL-17 and Thl7 cells in rheumatoid arthritis[ J]. Rheum Dis Clin North Am,2010,36(2) :345 -366.
  • 4Hochberg MC. Updating the American College of Rheumatology revised criteria for the classification of systemic lupus erythematosus [ J ]. Arthritis Rheum, 1997 ,d0 (9) : 1725.
  • 5Bombardier C, Gladman DD, Urowitz MB, et al. Derivation of the SLEDAI. A disease activity index for lupus patients. The committee on prognosis studies in SLE [ J ]. Arthritis Rheum, 1992,35(6) :630-640.
  • 6Dong C. Diversification of T-helper-cell lineages: finding the family root of IL-17-producing ceils [ J ]. Nat Rev Immunol, 2006,6(4) :329 - 333.
  • 7Wang CK, Ho CY, Li EK, et al. Elevation of proinflammatory eytokine ( IL-18, IL-17, IL-12 ) and Th2 eytokine ( IL-4 ) concentrations in patients with systemic lupus erythematosus [ J ]. Lupus,2000,9 ( 8 ) :589 - 593.
  • 8Wong CK, Lit LC, Tam LS, et al. Hyperproduction of IL-23 and IL-17 in patients with systemic lupus erythematosus: implications for Thl7-mediated inflammation in auto-immunity [ J ]. Clin Immunol,2008,127 ( 3 ) :385 - 393.
  • 9陈小奇,徐焱成,叶志勤,邓浩华,孙家忠,代喆,杨杪,吴玉文.RORrt基因表达和白细胞介素-17A与系统性红斑狼疮发病机制的初步研究[J].中华风湿病学杂志,2010,14(2):139-141. 被引量:1
  • 10Zhao XF,Pan HF,Yuan H,et al. Increased serum interleukin 17 in patients with systemic lupus erythematosus[ J]. Mol Biol Rep, 2010,37 ( 1 ) :81 - 85.

二级参考文献17

  • 1Seon Hee Chang.A novel heterodimeric cytokine consisting of IL-17 and IL-17F regulates inflammatory responses[J].Cell Research,2007,17(5):435-440. 被引量:48
  • 2Mosmann TR, Cherwinski H, Bond MW, et al, Two types of murine helper T cell clone: 1. definition according to profiles of lymphokine activities and secreted proteins. J Immunol, 1986, 136: 2438-2357.
  • 3Coffman RL, Cally JA. T cell activitity that enhances polyclonal IgE production and its inhibition by interferon-gamma. J Immunol, 1986, 136: 949-954.
  • 4Langrish CL, Chen Y, Blumenschein WM, et al. IL-23 drives a pathogenic T cell population that induces autoimmune inflammation. J Exp Med, 2005, 201: 233-:240.
  • 5Ivanov II, McKenzie BS, Zhou L, et al. The orphan nuelear receptor RORγt directs the differentiation program of proinflammatory IL-17^+ T helper cells. Cell, 2006, 126: 1121- 1133.
  • 6Harrington LE, Hatton RD, Mangzn PR, et al. IL-17 producing CD4^+ effector T cells develop via a lineage distinct from the T helper 1 and 2 lineages. Nat hnmunol, 2005, 6:1123-1132.
  • 7Lubberts E, Koenders MI, Oppers-Walgreen B, et al. Treatment with a neutralizing anti-murine inlerleukin-17 antibody after the onset of collagen-induced arthritis reduces joint inflammation, cartilage destruction and bone erosion. Arthritis Rheum, 2004, 50: 650-659.
  • 8Nurieva RI, Treuting P, Duong J, et al. Inducible eostimulator is essential for collagen-induced arthritis. J Clin Invest, 2003, 111: 701-706.
  • 9Nakae S, Nambu A, Sudo K, et al. Suppression of immune induction of collagen-induced arthritis in IL-17-deficient mice. J Immunol, 2003, 171: 6173-6177.
  • 10Wong CK, Ho CY, Li EK, et al. Elevation of proinflammatory eytokine (IL-18, IL-17, IL-12) and Th2 cytokine (IL-4) concentrations in patients with systemic lupus erythematosus. Lupus, 2000, 9: 589-593.

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