Authors: Q Yuan Y Zhao X Zhu X Liu
Publish Date: 2016/11/07
Volume: 40, Issue: 4, Pages: 397-407
Abstract
Graves’ disease GD is an autoimmune thyroid disease and the most important characteristic of it is the presence of the thyroidstimulating antibody TSAb The mechanisms of the TSAb elevation are still uncertain Recent studies have suggested that the dysregulation of regulatory T cell Treg and T helper 17 Th17 might stimulate the production of TSAb and be a pathogenesis of GD However the role of Treg and Th17 cells in the pathogenesis of GD is still debated Our aim is to assess changes of Treg and Th17 cells in the spleen of a mouse in an in vivo GD model and try to explain the pathogenesis of GDWe used an adenovirus expressing the autoantigen thyroidstimulating hormone receptor AdTSHR289 to immunise mice in order to induce GD in the model Flow cytometry was used to measure the frequencies of splenic Treg and Th17 cells and realtime PCR to analyse the mRNA expression of forkhead box P3Foxp3 and interleukin17IL17Compared with the AdControl group the frequencies of CD4+CD25+Foxp3+ Treg cells were significantly decreased p = 0007 and gene expression of Foxp3 was downregulated p = 0001 in the AdTSHR289 group Though there was no significant difference in CD4+IL17+ T cell subpopulation between the two groups p = 0336 the IL17 mRNA expression was significantly upregulated in the AdTSHR289 group p = 0001We thank Basil Rapoport University of CaliforniaLos Angeles for providing us with the plasmid of pSV2neoECETSHR2896Hdhfr We also thank National Natural Science Foundation of China for its generous support Grant No 81373593 without which our work would not have been possible
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