在小鼠中通过Lnc-Atg16l1的干环变化促进TLR7-MyD88依赖性炎症和自身免疫

Zongheng Yang1, Shuchen Ji1, Lun Liu1

  • 1Department of Immunology, Center for Immunotherapy, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, China.

Nature communications
|November 25, 2024
PubMed
概括

一种新的长非编码RNA,Lnc-Atg16l1,充当分子支架,使用结构变化来增强托尔类受体7 (TLR7) 信号传递. 这一发现为自身免疫性疾病机制和潜在的治疗点提供了新的见解.