期刊文献+

BLyS/April在川崎病患者中的表达及意义 被引量:2

Changes of BLyS/April in patients with Kawasaki disease
原文传递
导出
摘要 目的探讨BLyS/April在川崎病(KD)免疫发病机制中的作用。方法急性期KD患儿48例,正常同年龄对照组32名,KD患儿分别于静脉注射丙种球蛋白(IVIG)治疗前后直接取血备检。采用反转录-聚合酶链反应(RT-PCR)及荧光定量PCR检测单核-巨噬细胞(MC)BLyS和April,BLyS/April受体BR3、BCMA、TACI及细胞因子mRNA表达;双抗体夹心酶联免疫吸附试验(ELISA)检测血浆中细胞因子蛋白浓度。结果①急性期KD患儿MC BLyS和April mRNA表达明显高于正常同年龄对照组(P<0.01),经IVIG治疗后表达不同程度下降;②BLvS/April受体BR3、BCMA和TACI基因转录水平显著高于正常同年龄对照组(P<0.01);③急性期KD患儿抗体类型转换相关细胞因子白细胞介素(IL)-4、IL-5、IL-6、IL-10、IL-15 mRNA表达水平及蛋白浓度明显高于正常同年龄对照组(P<0.01);④KD患儿BLyS/April调控因子干扰素(IFN)-α/γ、IL-10 mRNA表达水平及血浆浓度明显高于正常同年龄对照组(P<0.01)。结论急性期KD患儿BLyS/April过表达可能是导致KD免疫功能紊乱的因素之一。 Objective To investigate the roles of BLyS/April in immunological pathogensis of Kawasaki disease (KD). Methods Forty-eight children with Kawasaki disease and 32 age-matched healthy children were studied. Reverse-transcription PCR(RT-PCR) and real-time PCR were used to measure the mRNA levels of BLyS/April, receptors for BLyS/April (BR3, BCMA and TACI) and cytokines in patients with KD. The levels of cytokines in plasma were measured by ELISA. Results ① Compared with healthy controls, transcription levels of BLyS/April in MC were significantly up-regulated during acute phase of KD (P〈0.01), and down-regulated after treated with intravenous immunoglobulin therapy. ② The expression levels of the BLyS/ April receptors BR3, BCMA and TACI mRNA were remarkably increased during acute phase of Kawasaki disease (P〈0.01), and down-regulated to some extents after treated with intravenous immunoglobulin therapy. ③The mRNA levels and plasma levels of cytokines such as IL-4, IL-5, IL-6, IL-10 and IL-15, which were in- volved in antibody class switching, were found to be significantly higher than those of healthy controls during acute phase of Kawasaki disease (P〈0.01). ④ The mRNA levels and the plasma levels of IL-10, IFN-α and 1FN-5,, were significantly elevated during acute phase of Kawasaki disease. Conclusion Overexpression of BLyS/April may be one contributing factor to the immunological dysfunction in KD.
出处 《中华风湿病学杂志》 CAS CSCD 2007年第6期331-334,共4页 Chinese Journal of Rheumatology
基金 国家自然科学基金(30571975) 深圳市科学技术项目基金(JH200505310548A)
关键词 黏膜皮肤淋巴结综合征 B淋巴细胞刺激因子 BLyS/April Mucocutaneous lymph node syndrome B lymphocyte stimulator
  • 相关文献

参考文献10

  • 1Fujieda M, Oishi N, Kurashige T.Antibodies to endothelial cells in Kawasaki disease lyse endothelial cells without cytokine pretreatment. Clin Exp Immunol, 1997, 107: 120-126.
  • 2Grunebaum E, Blank M, Cohen S,et al. The role of anti-endothelial cell antibodies in Kawasaki disease - in vitro and in vivo studies. Clin Exp Immunol, 2002, 130: 233-240.
  • 3Li CR, Yang XQ, Shen J, et al. Immunoglobulin G subclasses in serum and circulating immune complexes in patients with Kawasaki syndrome. Pediatr Infect Dis J, 1990, 9: 544-547.
  • 4Baker KP. BLyS: an essential survival factor for B cells: basic biology, links to pathology and therapeutic target. Autoimmun Rev, 2004,3: 368-375.
  • 5Schneider P. The role of APRIL and BAFF in lymphocyte activation. Curr Opin Immunol, 2005, 17: 282-289.
  • 6Theofilopoulos AN, Baeeala R, Beutler B, et al. Type Ⅰ interferons (alpha/beta) in immunity and autoimmunity. Annu Rev Immunol, 2005, 23: 307-336.
  • 7Mackay F, Browning JL. BAFF: a fundamental survival factor for B cells. Nat Rev Immunol, 2002, 2: 465-475.
  • 8Yazici ZA, Raschi E, Patel A, et al. Human monoclonal anti-endothelial cell IgG-derived from a systemic lupus erythematosus patient binds and activates human endothelium in vitro. Int Immunol, 2001, 13: 349-357.
  • 9王国兵,李成荣,祖莹,袁雄伟.Toll样受体信号途径活化在川崎病免疫发病机制中的作用[J].中华儿科杂志,2006,44(5):333-336. 被引量:23
  • 10王国兵,李成荣,祖莹,杨军,袁雄伟.Toll样受体信号途径负性调节因子在川崎病免疫发病机制中的作用[J].中华风湿病学杂志,2006,10(8):449-453. 被引量:9

二级参考文献9

共引文献25

同被引文献21

  • 1杜忠东,张永兰,赵地,杜军保,鲁珊,衣京梅,侯安存,周忠蜀,丁国芳,林瑶,刘冲,北京小儿川崎病流行病学调查协作组.静脉丙种球蛋白无反应性川崎病的治疗及危险因素分析[J].中国实用儿科杂志,2006,21(10):738-741. 被引量:89
  • 2Roberts PF,Waller TA,Brinker TM,et al.Henoche-Schonlein Purpura:a review article.South Med J,2007,100:821-824.
  • 3Eftychiou C,Sarnarkos M,Golfinopoulou S,et al.HenochSchonlein purpura associated with methicillin-resistant staphylococcus aureus infection.Am J Med,2006,119:85-86.
  • 4Reamy BV,Williams PM,Lindsay TJ.Henoch-Schonlein purpura.Am Fam Physician,2009,80:697-704.
  • 5Yang YH,Chuang YH,Wang LC,et al.The immunobiology of Henoch-Schonlein purpura.Autoimmun Rev,2008,7:179-184.
  • 6Arira S,Uematsu S,Takeuchi O.Pathogen recognition and innate immunity.Cell,2006,124:783-806.
  • 7Li M,Zhou Y,Feng G,et al.The critical role of Toll-like receptor signaling patlways in the induction and progression of autoimmune disease.Curr Mol Med,2009,9:356-374.
  • 8Marshak-Rothestein A.Toll-like receptor in systemic autoimmune disease.Nature Rev Immunol,2006,6:823-835.
  • 9Akira S.Pathogen recognition by innate immunity and its singnaling.Proc Jpn Acad Ser B Phys Biol Sci,2009,85:143-155.
  • 10Baccala R,Hoebe K,Kono DH,et al.TLR-dependent and TLRindependent pathways of type Ⅰ interferon induction in systemic autoimmunity.Nat Med,2007,13:543-551.

引证文献2

二级引证文献26

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部