抑制TBK1可释放RIPK1，使肿瘤对免疫疗法重新敏感。
TBK1 inhibition unleashes RIPK1, resensitizing tumors to immunotherapy.
作者信息
Kelliher Michelle A, Fitzgerald Katherine A
机构信息
Department of Molecular, Cell and Cancer Biology, University of Massachusetts Chan Medical School, University of Massachusetts, Worcester, MA, USA.
Division of Innate Immunity, University of Massachusetts Chan Medical School, University of Massachusetts, Worcester, MA, USA.
出版信息
Trends Immunol. 2023 Mar;44(3):156-158. doi: 10.1016/j.it.2023.01.009. Epub 2023 Feb 4.
Resistance mechanisms have curbed the potential of immune checkpoint blockade (ICB) therapies. Understanding mechanisms that contribute to this resistance should reveal new targets for combinatorial therapy. Tank-binding kinase 1 (TBK1) represents such a target. In recent work by Sun et al., inhibition of TBK1 restored the efficacy of such treatments by sensitizing tumors to RIPK1 kinase-dependent inflammatory cell death.
耐药机制限制了免疫检查点阻断（ICB）疗法的潜力。了解导致这种耐药性的机制应能揭示联合治疗的新靶点。 Tank结合激酶1（TBK1）就是这样一个靶点。在Sun等人最近的研究中，抑制TBK1通过使肿瘤对RIPK1激酶依赖性炎性细胞死亡敏感，恢复了此类治疗的疗效。
Zotero 插件