Toll样受体9（TLR9）在狼疮中触发不依赖髓样分化因子88（MyD88）的抗炎信号传导。

TLR9 triggers MyD88-independent anti-inflammatory signaling in lupus.

作者信息

Zhang Shikun, Cao Xuetao

机构信息

Department of Immunology, Institute of Basic Medical Sciences, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, China.

Department of Immunology, Institute of Basic Medical Sciences, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, China; Institute of Immunology, College of Life Sciences, Nankai University, Tianjin, China.

出版信息

Trends Immunol. 2023 Mar;44(3):153-155. doi: 10.1016/j.it.2023.01.008. Epub 2023 Feb 3.

DOI:10.1016/j.it.2023.01.008

PMID:36740514

Abstract

Activation of Toll-like receptor 7 (TLR7) can induce lupus in mice, whereas activation of TLR9 can prevent it, even though both receptors interact with myeloid differentiation primary response gene 88 (MyD88) for downstream signaling. How TLR9 triggers anti-inflammatory responses in autoimmunity is unclear. Leibler et al. recently reported that TLR9 initiates anti-inflammatory signaling and inhibits lupus pathogenesis in a MyD88-independent but ligand-dependent manner.

摘要

Toll样受体7（TLR7）的激活可在小鼠中诱发狼疮，而TLR9的激活则可预防狼疮，尽管这两种受体都与髓样分化初级反应基因88（MyD88）相互作用以进行下游信号传导。TLR9如何在自身免疫中触发抗炎反应尚不清楚。莱布勒等人最近报告称，TLR9以一种不依赖MyD88但依赖配体的方式启动抗炎信号传导并抑制狼疮发病机制。