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桥本甲状腺炎患者Th17细胞比例升高 被引量:9

Increased frequency of Th17 cell in patients with Hashimoto's thyroiditis
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摘要 目的研究桥本甲状腺炎(HT)患者Th17细胞及其相关因子的变化。方法选取30例桥本甲状腺炎患者,并以30名健康对照进行研究。Th17细胞采用流式细胞术测定,孤儿核受体γt(RORγt)和白细胞介素(IL)-17采用实时定量PCR测定,IL-6和IL-23采用ELISA法测定。结果(1)与健康对照相比,桥本甲状腺炎患者外周血中Th17细胞比例明显增加[(0.75±0.79)%对(0.28±0.23)%],RORγt水平增高(0.30±0.38对0.04±0.02,均P〈0.05);(2)桥本甲状腺炎患者血清中IL-6和IL-23水平显著高于健康对照组(3.66±4.70对0.47±1.11,154.7±75.81对80.65±61.41.均P〈0.05);(3)桥本甲状腺炎患者Th17细胞与甲状腺球蛋白抗体(TgAb)水平呈正相关(r=0.8484,P=0.0077);(4)桥本甲状腺炎患者甲状腺组织中表达RORγt和IL-17基因。结论桥本甲状腺炎患者体内Th17细胞及相关因子异常增高。 Objective To study the alteration of Thl7 cells and related molecules in patients with Hashimoto's thyroiditis ( HT). Methods Th17 cells were determined by flow cytometry. Real-time PCR method was applied to detect the expression of the orphan nuclear receptor RORγt and interleukin (IL) -17. Serum IL-6 and IL-23 were detected by ELISA method. Results ( 1 ) Compared with healthy controls, the frequency of Th17 cells [ (0.75 ± 0.79) % vs (0.28 ± 0.23 ) % ] and expression of RORγt ( 0, 30 + 0.38 vs 0. 04 ± 0.02, both P〈 0.05 ) were significantly increased in HT patients. (2) The levels of IL-6 and IL23 in HT patients were higher than those in healthy controls ( 3.66 ± 4.70 vs 0. 47±1.11, 154.7 ± 75.81 vs 80.65 ± 61.41, both P〈0.05 ). ( 3 ) A positive correlation between Thl 7 cells and serum TgAb was revealed in HT patients (r = 0. 848 4, P = 0. 007 7 ). (4) The results of PCR showed that IL-17 and RORγt expressed in thyroid tissues of patients HT. Conclusion An increased frequency of Th17 cells was found in HT patients, implying that this cell subset may play an important role in the pathogenesis of autoimmune thyroid disease.
出处 《中华内分泌代谢杂志》 CAS CSCD 北大核心 2012年第8期638-640,共3页 Chinese Journal of Endocrinology and Metabolism
基金 国家自然科学基金资助项目(30871193、30972748).江苏省卫生厅科研资助项目(H200952)
关键词 桥本甲状腺炎 TH17细胞 自身免疫 甲状腺 Hashimoto's thyroiditis Th17 cells Autoimmune diseases Thyroid gland
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参考文献10

  • 1王胜军,江淑芳,许化溪,柳龙图,刘恭植.桥本甲状腺炎患者甲状腺与外周血中单个核细胞免疫功能比较[J].中华内分泌代谢杂志,2000,16(2):99-101. 被引量:8
  • 2Ghureschi K, Laurence A, Yang XP, et al. T helper 17 cell heterogeneity and pathogenicity in autoimmune disease. Trends lmmunol, 2011,32:395-401.
  • 3Bettelli M, Oukka M, Kuchroo VK. TH-17 cells in the circle of immunity and autoimmunity. Nature hnnmnology, 2007,8:345-350.
  • 4Ivanov 11, lshigame H. The IL-23/IL-17 axis in inflaramaticm. J Clin Invest, 2006,116 : 1218-1222.
  • 5Langrish CL, Chen Y, Blumenschein WM, et al. 11,-23 drives a pathogenic T cell population thai induces autoimmune inflammation. J Exp Med, 2005,201:233-240.
  • 6Chen Y, Langrish CL, Mckenzie B, et al. Anti-lL-23 therapy inhilfits multiple inflammato pathways and ameliorates autoimnnme encephalomyelitis. J Clin Invest. 2006.116 : 1317-1326.
  • 7Komiyanm YS, Nakae S, Matsuki T. el al. IL-17 plays an ilnportaut role in the development of experimental autoinmmne encephalolny- etitis. J lmmunul, 2005,175:404-412.
  • 8Nishihara M, Ogura H, Ueda N, et al. IL-6-gpI30-STA3 in T cells directs the development of IL-17 + Th with a minimum effect on thai of Treg in the steady state. Int Immunul, 2007,19:695-702.
  • 9lvanov II, McKenzie BS, Zhou L, et al. The orphan nuclear receptor RORt directs the differentiation program of proifflammatoy 1L-17 + T helper cells. Cell, 2006,126:1121-1133.
  • 10Fujita-Sato S, lio S, lsobe T, et al. Slrnctural basis of digoxin that antagonizes RORgamma t receptor activity and suppresses Th17 cell differentiation and interleukin (11,)-17 production. J Biol Chem, 2011,286:31409-31417.

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