期刊文献+

NOD小鼠调节性T细胞的功能表型分析

Analysis on the function and phenotype of regulatory T cells in non-obese diabetic mice
下载PDF
导出
摘要 目的:比较和探讨NOD(Non-Obese Diabetic)小鼠与正常BALB/C小鼠脾脏中CD4^+CD25^+调节性T细胞(regulatory T cell,Treg)的功能表型分子、抑制性细胞因子的表达差异及意义。方法:采用流式细胞检测技术,测定NOD小鼠(实验组)和正常BALB/C小鼠(对照组)脾脏中Treg细胞(CD4^+CD25^+Foxp3^+)的比例、功能表型分子(CTLA-4、GITR)和抑制性细胞因子(IL-10、TGF-β)的表达比例和平均荧光强度(mean fluorescence intensity,MFI)。结果:NOD小鼠脾脏中CD4^+CD25^+Foxp3^+Treg细胞比例与对照组相比无显著差异,但Foxp3^+的MFI显著降低;NOD小鼠Treg细胞表达CTLA-4、GITR、IL-10、TGF-β均发生不同程度降低。结论:NOD小鼠Treg细胞功能表型分子表达下降,提示其免疫抑制功能降低,这可能与Ⅰ型糖尿病(typeⅠdiabetes mellitus,T1DM)的发病有一定关系。 Objective: To compare the expression of surface functional molecules and immunosuppressive cytokines( CD4~+CD25~+) of regulatory T cells( Tregs) in non-obese diabetic( NOD) mice and BALB /C mice. Methods: The percentage and expression intensity of key transcription factor Foxp3~+,surface molecules( CTLA-4,GITR) and cytokines( IL-10 and TGF-β) of CD4~+CD25~+Tregs in spleen of mice were determined with fluorescent antibody staining and analyzed by flow cytometry. Results: There was no significant difference in the percentage of CD4~+CD25~+Foxp3~+Tregs between NOD and control mice. However,CD4~+CD25~+Tregs in NOD mice had led to significantly reduced expression levels of Foxp3~+,surface molecules( CTLA-4,GITR) and cytokines( IL-10 and TGF-β),when expressed as the mean fluorescence intensity( MFI) respectively. Conclusion: Our findings confirmed impaired function of CD4~+CD25~+Tregs in NOD mice that may facilitate the pathogenesis of T1 DM.
作者 吴玲
出处 《皖南医学院学报》 CAS 2016年第3期219-222,共4页 Journal of Wannan Medical College
关键词 1型糖尿病 NOD小鼠 调节性T细胞 type 1 diabetes mellitus non-obese diabetic mice regulatory T cell
  • 相关文献

参考文献1

二级参考文献92

  • 1Sakaguchi S, Sakaguchi N, Asano M, Itoh M, Toda M. Immunologic self-tolerance maintained by activated T cells expressing IL-2 receptor alpha-chains (CD25). Breakdown of a single mechanism of self-tolerance causes various autoimmune diseases. J Immunol 1995; 155: 1151-1164.
  • 2Wing K, Sakaguchi S. Regulatory T cells exert checks and balances on self tolerance and autoimmunity. Nat Immuno12010; 11: 7-13.
  • 3Littman DR, Rudensky AY. Th17 and regulatory T cells in mediating and restraining inflammation. Ce112010; 140: 845-858.
  • 4Campbell D J, Koch MA. Phenotypical and functional specialization of FOXP3+ regulatory T cells. Nat Rev Immuno12011; 11:119-130.
  • 5Feuerer M, Hill JA, Mathis D, Benoist C. Foxp3+ regulatory T cells: differentiation, specification, subphenotypes. Nat Immunol 2009; 10: 689-695.
  • 6Fontenot JD, Gavin MA, Rudensky AY. Foxp3 programs the develop- ment and function of CD4+CD25+ regulatory T cells. Nat Immunol 2003: 4: 330-336.
  • 7Fontenot JD, Gavin MA, Rudensky AY. Foxp3 programs the develop- ment and function of CD4CD25+ regulato T cells. Nat Immunol 2003;4:330-336.
  • 8Khattri R, CoxT, Yasayko SA, Ramsdell F. An essential role for Scurfin in CD4+CD25+ T regulatory cells. Nat Immuno12003; 4: 337-342.
  • 9Brunkow ME, Jeffery EW, Hjerrild KA, Paeper B, Clark LB, Yasayko SA et al. Disruption of a new forkhead/winged-helix protein, scurfin, results in the fatal lymphoproliferative disorder of the scurfy mouse. Nat Genet 2001; 27: 68-73.
  • 10Bennett CL, Christie J, Ramsdell F, Brunkow ME, Ferguson P J, Whitesell Let al. The immune dysregulation, polyendocrinopathy, enteropathy, X-linked syndrome (IPEX) is caused by mutations of FOXP3. Nat Genet2001; 27: 20-21.

共引文献35

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