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RelB regulates the homeostatic proliferation but not the function of Tregs

机译:Relb调节稳态增殖,但不是Tregs的功能

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RelB, a member of the NF-κB family, plays a critical role in the development of T cells. However, the role of RelB in Foxp3+ regulatory T cells (Tregs) remains controversial. Using a bone marrow chimeric mouse model, we demonstrated that the expansion of Foxp3+ Tregs in vivo could be mediated by extrinsic mechanisms. RelB plays an important role in inhibiting the homeostatic proliferation of Tregs, but not their survival. Even with the heightened expansion, RelB?/? Treg cells displayed normal suppressive function in vitro. Among the expanded populations of Treg cells, most were nTreg cells; however, the population of iTregs did not increase. Mechanistically, RelB seems to regulate Treg proliferation independently of the signal transducer and activator of transcription 5 (STAT5) pathway. These data suggest that RelB regulates Treg proliferation independently of the STAT5 pathway, but does not alter the function of Tregs. Further studies are warranted to uncover such mechanisms.
机译:Relb是NF-κB系列的成员,在T细胞的发展中起着关键作用。然而,Relb在FoxP3 +调节T细胞(Tregs)中的作用仍然存在争议。使用骨髓嵌合小鼠模型,我们证明了体内Foxp3 + Tregs的扩增可以通过外在机制来介导。 Relb在抑制Tregs的稳态增殖中起重要作用,但不是它们的存活率。即使加强扩张,Relb?/? Treg细胞在体外显示正常抑制功能。在Treg细胞的扩增群体中,大多数是Ntreg细胞;但是,ITREGS的人口没有增加。机械地,RelB似乎可以通过单独的信号传感器和转录5(STAT5)途径的激活剂来调节Treg增殖。这些数据表明,Relb调节Treg扩散独立于Stat5路径,但不会改变Tregs的功能。进一步研究是为了发现此类机制。

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