Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA.
Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA; Howard Hughes Medical Institute, Yale University, New Haven, CT 06520, USA.
Mol Cell. 2014 Dec 18;56(6):719-20. doi: 10.1016/j.molcel.2014.12.010.
In this issue, Xu et al. (2014) show that innate antiviral RIG-I-like receptors (RLR) signaling represses TGF-β-induced growth inhibition, epithelial-mesenchyme transition (EMT), and regulatory T cell (Treg) differentiation via IRF3-mediated Smads function.
在本期中,徐等人(2014 年)表明,先天抗病毒 RIG-I 样受体(RLR)信号通过 IRF3 介导的 Smads 功能抑制 TGF-β诱导的生长抑制、上皮间质转化(EMT)和调节性 T 细胞(Treg)分化。