cGAS and DDX41-STING mediated intrinsic immunity spreads intercellularly to promote neuroinflammation in SOD1 ALS model

Hong Yien Tan, Yean Kong Yong, Yuan Chao Xue, Huitao Liu, Tomomi Furihata, Esaki Muthu Shankar, Chen Seng Ng (Leading Author)

Research output: Contribution to journalArticleResearchpeer-review

38 Citations (Scopus)

Abstract

Neuroinflammation exacerbates the progression of SOD1-driven amyotrophic lateral sclerosis (ALS), although the underlying mechanisms remain largely unknown. Herein, we demonstrate that misfolded SOD1 (SOD1Mut)-causing ALS results in mitochondrial damage, thus triggering the release of mtDNA and an RNA:DNA hybrid into the cytosol in an mPTP-independent manner to activate IRF3- and IFNAR-dependent type I interferon (IFN-I) and interferon-stimulating genes. The neuronal hyper-IFN-I and pro-inflammatory responses triggered in ALS-SOD1Mut were sufficiently robust to cause a strong physiological outcome in vitro and in vivo. cGAS/DDX41-STING-signaling is amplified in bystander cells through inter-neuronal gap junctions. Our results highlight the importance of a common DNA-sensing pathway between SOD1 and TDP-43 in influencing the progression of ALS.

Original languageEnglish
Article number104404
Number of pages42
JournaliScience
Volume25
Issue number6
DOIs
Publication statusPublished - 17 Jun 2022
Externally publishedYes

Keywords

  • Immunology
  • Neuroscience
  • Pathophysiology

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