ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Type I Interferon Signaling Augments Autoimmunity in Neuromyelitis Optica Spectrum Disorder.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- The cGAS-STING pathway: mechanistic basis, dual biological functions and translational therapeutic advances.Apoptosis : an international journal on programmed cell death · 2026Review
- Natural killer cell reduction and dysfunction define a pathogenic and diagnostic axis in neuromyelitis optica spectrum disorder.Journal of neuroinflammation · 2026Article
- An autoinflammatory RIG-I variant causing Singleton-Merten syndrome associates with small non-coding Y-RNAs.Discovery immunology · 2026Article
- AQP4+ NMOSD, MDA5+ Clinically Amyopathic Dermatomyositis and sHLH in a Pediatric Patient: A Case Report and Literature Review.Journal of inflammation research · 2026Article
- Type I Interferon Signaling Augments Autoimmunity in Neuromyelitis Optica Spectrum Disorder.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
Corrections and comments
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Authors and funding
14 authors.
Funding
Abstract
Neuromyelitis optica spectrum disorder (NMOSD) is an autoimmune disease characterized by anti-aquaporin 4 (AQP4) antibody-mediated astrocyte damage and subsequent demyelination. Prior attempts to treat NMOSD with interferon-beta (IFN-β), a disease-modifying therapy for multiple sclerosis, resulted in worsening of disease activity, with an unknown mechanism. Here, robust activation of the cGAS-STING-IFN-I signaling pathway is identified in myeloid cells in both the periphery and central nervous system. The abnormal IFN-I response gives rise to an increase in the number of AQP4 antigen-specific autoreactive T cells. Sting deficiency can significantly blunt the activation of AQP4-specific T cells, as well as the IFN-I activity in microglia, and attenuate astrocyte damage. Consequently, the clinical manifestation of NMOSD is ameliorated in a passive transfer mouse model of NMOSD. Further, treatment with STING inhibitor H151 alleviates the severity of NMOSD mouse models. These findings uncover the cGAS-STING-IFN-I pathway in promoting autoreactive T cells and establish a foundation for inhibiting this pathway as a new therapeutic revenue for NMOSD.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.