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  • 标题:Programmed death one homolog maintains the pool size of regulatory T cells by promoting their differentiation and stability
  • 本地全文:下载
  • 作者:Qi Wang ; Jianwei He ; Dallas B. Flies
  • 期刊名称:Scientific Reports
  • 电子版ISSN:2045-2322
  • 出版年度:2017
  • 卷号:7
  • 期号:1
  • DOI:10.1038/s41598-017-06410-w
  • 语种:English
  • 出版社:Springer Nature
  • 摘要:Programmed death one homolog (PD-1H) is an immunoglobulin superfamily molecule and primarily acts as a coinhibitor in the initiation of T cell response to antigens. Here, we report that genetic ablation of PD-1H in mice blocks the differentiation of naive T cells to Foxp3(+) inducible Treg cells (iTreg) with a significant decrease of iTreg in lymphoid organs. This effect of PD-1H is highly specific for iTreg because both naturally generated iTreg in gut-related tissues and in vitro induced iTreg by TGF-β were decreased whereas the genesis of natural Treg (nTreg) remains normal. The suppressive function of both iTreg and nTreg, however, is not affected by the loss of PD-1H. In addition to decreased production, PD-1H deficient iTreg could also rapidly convert to CD4(+) T helper 1 or T helper 17 cells in an inflammatory environment. Our results indicate that PD-1H is required for maintenance of iTreg pool size by promoting its differentiation and preventing its conversion to other CD4(+) T cell subsets. These findings may have important implications for manipulating Tregs to control inflammation.
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