期刊文献+

儿童自身免疫性甲状腺疾病发病机制的研究进展 被引量:6

Research Progress in Pathogenesis of Childhood Autoimmune Thyroid Disease
下载PDF
导出
摘要 自身免疫性甲状腺疾病(AITD)主要包括毒性弥漫性甲状腺肿和桥本甲状腺炎。儿童AITD发病率较成人低,但有逐年升高趋势,且儿童AITD临床症状较重,影响生长发育,病情易反复,不易治愈,已成为危害我国儿童健康的一种慢性病。AITD的发病机制尚未完全明确,目前认为是由遗传易感性和环境诱因共同作用于机体免疫系统,破坏自身免疫耐受引起。AITD的免疫失衡过程由甲状腺自身抗体、T细胞及B细胞共同参与,其中辅助性T细胞(Th) 1和Th2细胞、Th17和调节性T细胞之间的平衡,以及滤泡辅助性T淋巴细胞、Th9、Th22和B细胞,均在AITD的发病机制中起重要作用。因此,深入探索儿童AITD的发病机制,可为将来开发AITD的免疫调节或免疫靶向治疗提供依据。 Autoimmune thyroid disease( AITD) mainly includes toxic diffuse goiter and Hashimoto thyroiditis.Although the incidence of AITD in children is much lower than that in adults,it is gradually increasing year by year.Children AITD has severe clinical symptoms,which affects growth and development,is prone to relapse,and difficult to cure,and has become a chronic disease endangering children’s health in China.The pathogenesis of AITD remains unclear.Currently,it is believed that the disease is caused by the combination of genetic susceptibility and environmental factors,which both act on the immune system and destroy the autoimmune tolerance.Thyroid autoantibodies,T cells and B cells are involved in the immune imbalance process of AITD.The balance between helper T cell( Th) 1 and Th2 cell,Th17 and regulatory T cell,as well as T follicular helper cell,Th9,Th22 and B cell,all play an important role in the pathogenesis of AITD.Therefore,in-depth exploration of the pathogenesis of AITD in children can provide the basis for the development of immunomodulator or immunotargeted therapy for AITD in the future.
作者 夏秦 陈临琪 陈婷 XIA Qin;CHEN Linqi;CHEN Ting(Department of Endocrinology,Genetics and Metabolism,Children′s Hospital of Soochow University,Suzhou 215000,China)
出处 《医学综述》 2021年第3期428-435,441,共9页 Medical Recapitulate
基金 国家自然科学基金(81700793) 姑苏卫生人才培养项目(GSWS2019051)。
关键词 自身免疫性甲状腺疾病 儿童 发病机制 毒性弥漫性甲状腺肿 桥本甲状腺炎 Autoimmune thyroid disease Children Pathogenesis Toxic diffuse goiter Hashimoto thyroiditis
  • 相关文献

参考文献10

二级参考文献142

  • 1Lee YH, Rho YH,Choi SJ, et al. The PTPN22 C1858T functional polymorphism and autoimmune diseases--a meta-analysis. J Rheumatol,2007,46:49-56.
  • 2Criswell LA, Pfeiffer KA, Lum RF, et al. Analysis of families in the multiple autoimmune disease genetics consortium (MADGC) collection: the PTPN22 620W allele associates with multiple autoimmune phenotypes. J Hum Genet, 2005,76: 561-571.
  • 3Velaga MR,Wilson V,Jennings CE,et al.The codon 620 tryptophan allele of the lymphoid tyrosine phosphatase (LYP) gene is a major determinant of Graves' disease. J Clin Endocrinol Metab, 2004, 89: 5862-5865.
  • 4Hill RJ, Zozulya S, Lu YL, et al. The lymphoid protein tyrosine phosphatase Lyp interacts with the adaptor molecule Grh2 and functions as a negative regulator of T-cell activation. J Exp Hematol, 2002, 30: 237-244.
  • 5Mustelin T, Alonso A, Bottini N, et al. Protein tyrosine phosphatases in T cell physiology.J Mol Immunol,2004,41:687-700.
  • 6Ladner MB, Bottini N, Valdes AM, et al. Association of the single nucleotide polymorphism C1858T of the PTPN22 gene with type 1 diabetes.J Hum Immunol,2005,66:60-64.
  • 7Hermann K, Lipponen M, Kiviniemi T, et al.Lymphoid tyrosine phosphatase (LYP/PTPN22) Arg620Trp variant regulates insulin autoimmunity and progression to type 1 diabetes. Diabetologia, 2006, 49: 1198-1208.
  • 8Bottini N, Musumeci L,Alonso A,et al.A functional variant of lymphoid tyrosine phosphatase is associated with type 1 diabetes. J Nat Genet,2004,36: 337-338.
  • 9Begovich AB, Carlton VE, Honigberg LA, et al. A missense single-nucleotide polymorphism in a gene encoding a protein tyrosine phosphatase(PTPN22) is associated with rheumatoid arthritis. J Hum Genet, 2004,75 : 330-337.
  • 10Hasegawa K, Martin F, Huang G, et al. PEST domain-enriched tyrosine phosphatase (PEP) regulation of effector/memory T cells. Science,2004,303:685-689.

共引文献94

同被引文献52

引证文献6

二级引证文献19

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