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慢性荨麻疹患者血清IL-35水平检测分析 被引量:6

Analysis of IL-35 in serm from patients with chronic urticaria
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摘要 目的探讨IL-35在慢性荨麻疹患者致病机制中的作用。方法根据自身血清皮肤试验(ASST)将慢性慢性荨麻疹患者分成两组,应用ELISA法检测两组患者血清IL-35、IL-23浓度,流式细胞仪检测患者外周血细胞免疫功能,同时设立对照组进行比较。结果 53例慢性荨麻疹患者中,33例患者ASST测试结果为阳性,20例为阴性;两组患者与对照组比较血清IL-35浓度均升高,IL-23浓度降低(P<0.01);外周血CD8+细胞降低(P<0.05);B细胞降低,差异有统计学意义,其中ASST阳性组B细胞降低更为明显。结论慢性荨麻疹患者机体可能存在Th17/Treg(调节性T细胞)不平衡,导致病情反复迁延。 Objective To explore the significance of the detection of serum level of IL-35 for pathogenic mechanisms in the pa- tients with chronic urticaria. Methods 3 patients with chronic urticaria based on the ASST test results were divided into positive and negative groups. ELISA assay in CU IL-23, IL-35 content,and the flow cytometry was used to detect T lymphocyte subsets, NK cells,B cells,while the establishment of normal control group. Results Of the 53 patients in patients with CU,33(62.26%) were positive for ASST, 20(37.74 %)were negative for ASST. Serum levels of IL-35 in patients with CU were significantly higher than the control normal group,and IL-23 level was lower(P〈0.01). The percentage of CD8+ .13 cells were lower in the patients with CU,and the ratio of CD4+/CD8+ was higher(P^0.05). B cells decreased, the difference was statistically significant, in which ASST positive group was lower in B cells. Conclusion The imbalance of Thl7/Treg(Regulatory T-cells Treg) was probably one of the immunical pathogenesis with CU.
出处 《国际检验医学杂志》 CAS 2013年第7期786-786,788,共2页 International Journal of Laboratory Medicine
基金 广东省广州市医药科技卫生资助项目(2009-YB-233)
关键词 荨麻疹 血清 酶联免疫吸附测定 urticaria i serum i enzyme-linked immunosorbent assay
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  • 1Greaves M. Chronic urticaria. J Allergy Clin Immunol 2000; 105 (4) :664 - 672.
  • 2Grattan CE, Francis DM, Hide M, et al. Detection of circulating histamine releasing anteantibodies with functional properties of anti -IgE in chronic urticaria. Clin Exp Allergy 1991;21(6):695- 704.
  • 3Kaplan AP. Chronic urticaria: Pathogenesis and treatment. J Allergy Clin Imrnunol 2004; 114(3) :465 - 474.
  • 4Brunetti L, Francavilla R, Miniello VL, et al. High prevalence of autoimmune urticaria in children with chronic urticaria. J Allergy Clin Immunol 2004; 114(4) :922- 927.
  • 5Soundararajan S, Kikuchi K, Joseph K, et al. Functional assessment of pathogenic IgG subclasses in chronic autoimmune urticaria. J Allergy Clin Immunol 2005 ; 115(4) : 815 - 821.
  • 6Hide M, Francis DM, Grattan CEH, et al. Autoantibodies against the high affinity IgE receptor as a cause for histamine release in chronic urticaria. New Eng J Med 1993;328(22) :1599 - 1604.
  • 7Nimii N, Francis DM, Kermani F, et al. Dermal mast cell activation by autoantibody against the high affinity IgE receptor in chronic urticaria. J Invest Dermatol 1996; 106(5) : 1001 - 1006.
  • 8Sabroe RA, Fiebiger E, Francis DM, et al. Classification of anti - FcepsilonRI and anti - IgE autoantibodies in chronic idiopathic urticaria and correlation with disease severity. J Allergy Clin Immunol 2002; 110(3):492 - 499.
  • 9Yasnowsky KM, Dreskin SC, Efaw B, et al. Chronic urticaria sera increase basophil CD203c expression. J Allergy Clin Immunol 2006; 117(6) : 1430 - 1434.
  • 10Frezzolini A, Provini A, Teofoli P, et al. Serum - induced basophil CD63 expression by means of a tricolour flow cytometric method for the in vitro diagnosis of chronic urticaria. Allergy 2006;61 (9) : 1071 - 1077.

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  • 1张敏,李春阳.Thl-Th2失衡与慢性荨麻疹[J].临床皮肤科杂志,2005,34(5):336-337. 被引量:55
  • 2Collison LW, Workman C J, Kuo Tr,et al. The inhibitory eytokine IL- 35 contributes to regulatory T cell function [ J ]. Nature, 2007,450 ( 169 ) :566-569.
  • 3Chaturvedi V, Collison LW, Guy CS, et al. Cutting edge: Human regu- latory T cells require IL-35 to mediate suppression and infectious toler- ance [ J ]. J Immuno1,2011,186 ( 12 ) :6661-6666.
  • 4Jones LL, Vignali DA. Molecular interactions within the IL-6/IL-12 cytokine/receptor superfamily [ J ]. Immounol Res, 2011,51 ( 1 ) : 5- 14.
  • 5Collison LW, Delgoffe GM, Guy CS, et al. The composition and signa- ling of the IL-35 receptor are unconventional [ J ]. Nat Immunol,2012, 13 ( 3 ) :290-299.
  • 6Collison LW, Chaturvedi V, Henderson AL, et al. IL-35-mediated in- duction of a potent regulatory T cell population [ J ]. Nat Immunol, 2010,11 ( 12 ) : 1093-1101.
  • 7Niedbala W, Wei XQ, Cai B, et al. IL-35 is a novel cytokine with ther- apeutic effects against collagen- induced arthritis through the expan- sion of regulatory T cells and suppression of Thl7cells [ J ]. Eur Immu- nol,2007,37( 11 ) :3021-3029.
  • 8Kochetko'ca I, Golden S, I-Ioldemess K, et al. IL-35 stimulation of CD39 + regulatory T cells confers protection against collagen Ⅱ-in- duced arthritis via the production of IL-10 [ J ]. Immunol, 2010,184 (12) :1144-1153.
  • 9Kuo J, Nardelli DT, Warner TF, et al. Interleukin-35 enhances Lyme arthritis in Borrelia-vaecinated and-infected mice [ J ]. Clin Vaccine Immunol,2011,18(7) :1125-1132.
  • 10Whitehead GS,Wilson RH,Nakano K, et al. IL-35 production by in- ducible costimulator(ICOS)-positive regulatory T cells reverses es- tablished IL-17 dependent allergic airways disease[ J]. J Allergy Clin Immunol,2012,129 ( 1 ) :207-215.

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