期刊文献+

Tet调控Th17/Treg细胞分化参与自身免疫性疾病发病的研究进展

Tet in regulation of Th17/Treg cell differentiation and in participatesion of pathogenesis of autoimmune diseases
下载PDF
导出
摘要 CD4^(+)T细胞是人体免疫重要的一部分,其中辅助性T细胞17(T helper cell 17,Th17)和调节性T细胞(regulatory T cells,Treg)两个新近发现的CD4^(+)T细胞亚群在自身免疫疾病的发生发展中也起关键作用。Th17细胞能够引起自身免疫和炎性反应,而Treg细胞抑制疾病发生并维持免疫稳态;10~11易位蛋白(ten-eleven translocation,Tet)作为DNA去甲基化的关键因子,当其缺失时能够影响Th17/Treg免疫平衡。本文针对Tet调控Th17/Treg细胞分化参与自身免疫疾病发生发展的研究进展作一综述。 CD4^(+)T cells are an important part of human immunity.T helper cell 17(Th17)and regulatory T cells(Treg),two newly discovered subsets of CD4^(+)T cells,play a key role in the occurrence and development of autoimmune diseases.Th17 cause autoimmunity and inflammation,while Treg inhibit the emergence of diseases and maintain immune homeostasis.Ten-eleven translocation(Tet),as a key factor in DNA demethylation,affects the Th17/Treg balance and involves in the progression of autoimmune diseases when it is absent.This review focuses on the research of the regulatory role of Tet on Th17/Treg cell immunization balance and the possible pathogenesis of autoimmune diseases.
作者 姜冠桐 周瑾 薛海波 Jiang Guantong;Zhou Jin;Xue Haibo(Department of Endocrinology,Binzhou Medical University Hospital,Binzhou 256603,China;Department of Endocrinology,Yantai Yuhuangding Hospital,Yantai 264000,China)
出处 《国际医药卫生导报》 2022年第11期1500-1504,共5页 International Medicine and Health Guidance News
基金 山东省研究生教育创新计划项目(20038612) 滨州医学院附属医院科研创新团队(202031) 滨州医学院附属医院后备领军人才(JC2019-03)。
关键词 TET TH17 TREG TH17/TREG 自身免疫性疾病 Tet Th17 Treg Th17/Treg Autoimmune diseases
  • 相关文献

参考文献3

二级参考文献20

  • 1Prabhakar BS, Balm RS, Smith pathogenesis of Graves' disease TJ. Current perspective on the and ophthalmopathy [J]. Endocr Rev, 2003, 24(6): 802-35.
  • 2Brent GA. Graves'disease [J]. N Engl J Med, 2008, 358(24): 2594-605.
  • 3Josefowicz SZ, Lu LF, Rudensky AY. Regulatory T cells: mechanisms of differentiation and function[J]. Ann Rev Immunol, 2012, 30: 531-64.
  • 4Bettelli E, Cartier Y, Gao W, et al. Reciprocal developmental pathways for the Generation of pathogenic effector TH17 and regulatory T cells[J]. Nature, 2006, 441(790): 235-8.
  • 5Su CG, Wen X, Bailey ST, et al. A novel therapy for colitis utilizing PPAR-gamma ligands to inhibit the epithelial inflammatory response[J]. J Clin Invest, 1999, 104(4): 383-9.
  • 6Lewis JD, Lichtenstein GR, Stein RB, et al. An open-label trial of the PPAR gamma ligand rosiglitazone for active ulcerative colitis [J]. Am J Gastroenterol, 2001, 96(12): 3323-8.
  • 7Balm RS. Pathophysiology of graves'ophthalmopathy: the cycle of disease[J]. J Clin Endocrinol Metab, 2003, 88(5): 1939-46.
  • 8Drexhage HA. Are there more than antibodies to the thyroid- stimulating hormone receptor that meet the eye in Graves' disease? [J]. Endocrinology, 2006, 147(1): 9-12.
  • 9Pappa A, Calder V, Ajjan R, et al. Analysis of extraocularmuscle-infiltrating T cells in thyroid-associated ophthalmopathy (Tao) [J]. Clin Exp Immunol, 1997, 109(2): 362-9.
  • 10Aniszewski JP, Valyasevi RW, Balm RS. Relationship between disease duration and predominant orbital T cell subset in Graves' ophthalmopathy[J]. J Clin Endocrinol Metab, 2000, 85(2): 776-80.

共引文献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