Cerneckis Jonas, Shi Yanhong
Department of Neurodegenerative Diseases, Beckman Research Institute of City of Hope, Duarte, CA 91010, USA; Irell & Manella Graduate School of Biological Sciences, Beckman Research Institute of City of Hope, Duarte, CA 91010, USA.
Department of Neurodegenerative Diseases, Beckman Research Institute of City of Hope, Duarte, CA 91010, USA.
Trends Mol Med. 2025 Sep 10. doi: 10.1016/j.molmed.2025.08.007.
It is well established that pseudouridine (Ψ) and its derivative N-methylpseudouridine (mΨ) suppress unwanted immunogenicity of RNA-based therapeutics. However, molecular mechanisms governing such immune evasion remain elusive. In a recent article, Bérouti, Wagner, and colleagues show that Ψ impairs the processing of Toll-like receptor (TLR)-agonistic ligands and hinders TLR activation.
众所周知,假尿苷(Ψ)及其衍生物N-甲基假尿苷(mΨ)可抑制基于RNA的治疗药物产生不必要的免疫原性。然而,控制这种免疫逃逸的分子机制仍然不清楚。在最近的一篇文章中,贝鲁蒂、瓦格纳及其同事表明,Ψ会损害Toll样受体(TLR)激动剂配体的加工过程,并阻碍TLR激活。