Klunker Sven, Chong Mark M W, Mantel Pierre-Yves, Palomares Oscar, Bassin Claudio, Ziegler Mario, Rückert Beate, Meiler Flurina, Akdis Mübeccel, Littman Dan R, Akdis Cezmi A
Swiss Institute of Allergy and Asthma Research Davos, University of Zurich, CH-7270 Davos-Platz, Switzerland.
J Exp Med. 2009 Nov 23;206(12):2701-15. doi: 10.1084/jem.20090596. Epub 2009 Nov 16.
Forkhead box P3 (FOXP3)(+)CD4(+)CD25(+) inducible regulatory T (iT reg) cells play an important role in immune tolerance and homeostasis. In this study, we show that the transforming growth factor-beta (TGF-beta) induces the expression of the Runt-related transcription factors RUNX1 and RUNX3 in CD4(+) T cells. This induction seems to be a prerequisite for the binding of RUNX1 and RUNX3 to three putative RUNX binding sites in the FOXP3 promoter. Inactivation of the gene encoding RUNX cofactor core-binding factor-beta (CBFbeta) in mice and small interfering RNA (siRNA)-mediated suppression of RUNX1 and RUNX3 in human T cells resulted in reduced expression of Foxp3. The in vivo conversion of naive CD4(+) T cells into Foxp3(+) iT reg cells was significantly decreased in adoptively transferred Cbfb(F/F) CD4-cre naive T cells into Rag2(-/-) mice. Both RUNX1 and RUNX3 siRNA silenced human T reg cells and Cbfb(F/F) CD4-cre mouse T reg cells showed diminished suppressive function in vitro. Circulating human CD4(+) CD25(high) CD127(-) T reg cells significantly expressed higher levels of RUNX3, FOXP3, and TGF-beta mRNA compared with CD4(+)CD25(-) cells. Furthermore, FOXP3 and RUNX3 were colocalized in human tonsil T reg cells. These data demonstrate Runx transcription factors as a molecular link in TGF-beta-induced Foxp3 expression in iT reg cell differentiation and function.
叉头框蛋白P3(FOXP3)(+)CD4(+)CD25(+)诱导性调节性T(iT reg)细胞在免疫耐受和内环境稳态中发挥重要作用。在本研究中,我们发现转化生长因子-β(TGF-β)可诱导CD4(+)T细胞中与Runt相关的转录因子RUNX1和RUNX3的表达。这种诱导似乎是RUNX1和RUNX3与FOXP3启动子中三个假定的RUNX结合位点结合的先决条件。小鼠中编码RUNX辅因子核心结合因子-β(CBFβ)的基因失活以及人T细胞中通过小干扰RNA(siRNA)介导的RUNX1和RUNX3抑制导致Foxp3表达降低。在将Cbfb(F/F)CD4-cre幼稚T细胞过继转移到Rag2(-/-)小鼠中时,幼稚CD4(+)T细胞在体内向Foxp3(+)iT reg细胞转化的能力显著降低。RUNX1和RUNX3的siRNA均使人类T reg细胞沉默,并且Cbfb(F/F)CD4-cre小鼠T reg细胞在体外显示出抑制功能减弱。与CD4(+)CD25(-)细胞相比,循环中的人类CD4(+)CD25(高)CD127(-)T reg细胞显著表达更高水平的RUNX3、FOXP3和TGF-β mRNA。此外,FOXP3和RUNX3在人类扁桃体T reg细胞中共定位。这些数据表明Runx转录因子是TGF-β诱导的iT reg细胞分化和功能中Foxp3表达的分子纽带。