CSL(CBF1, Su(H) and LAG-1)-dependent Hes-1 signaling plays an important part in regulating Th17 cell differentiation. However, little is known about influence of CSL-independent Deltex-1 signaling on this subset. The current focus is on roles of the Deltex-1 signaling in the Th17 cell differentiation. IL-17-producing CD4⁺ T cell subpopulation could be induced in vitro by treatment of both IL-6 and TGF-β. This could be reversed by knockdown of the deltex-1 gene, following the attenuation of retinoic acid-related orphan receptor γt (RORγt) and its DNA-binding activity in nuclei. Subsequently, Th17-associated cytokines generated by the treated cells were also diminished by the inhibition of Deltex-1 signaling, but the production of IL-10 was enhanced. Contrary to the alteration of RORγt, both zinc-finger transcription factor-3 (GATA3) and transcription factor Forkhead box P3 (Foxp3) were augmented at their mRNA and protein levels as well as DNA-binding activities with the emerging phenotypes of the corresponding cellular subpopulation and T-bet (encoded by TBX21) was not changed. These results reveal for the first time that Deltex-1 is indispensible for the IL-6 and TGF-β treatment-triggered differentiation of Th17 cells, indicating that CSL-independent Deltex-1 signaling favors naïve CD4⁺ T cells to deviate into Th17 cells via the enhancement of RORγt/IL-17A.

CSL（CBF1，Su（H）和LAG-1）依赖的Hes-1信号传导在调节Th17细胞分化中起重要作用。但是，关于CSL独立的Deltex-1信号对此子集的影响知之甚少。目前的重点是在Deltex-1信号在Th17细胞分化中的作用。IL- 6和TGF-β均可在体外诱导产生IL-17的CD4 ⁺ T细胞亚群。这可以通过删除deltex-1来逆转视黄酸相关孤儿受体γt（RORγt）的减弱及其在细胞核中的DNA结合活性。随后，通过抑制Deltex-1信号转导也减少了由处理过的细胞产生的与Th17相关的细胞因子，但IL-10的产生增加了。与RORγt的变化相反，锌指转录因子3（GATA3）和转录因子叉头盒P3（Foxp3）在其mRNA和蛋白质水平以及与相应细胞的新兴表型结合的DNA结合活性方面均得到增强。亚群和T- bet（由TBX21编码）未更改。这些结果首次揭示，Deltex-1对于IL-6和TGF-β治疗触发的Th17细胞分化是必不可少的，这表明不依赖于CSL的Deltex-1信号倾向于使幼稚的CD4 ⁺ T细胞偏离Th17细胞。通过增强RORγt/ IL-17A。