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The IL-1β-STING Signaling Axis Drives Neuromyelitis Optica Pathogenesis in a Murine Model.

Siyu Han1,2, Ziqi Liang3, Chongyou Zhang2

  • 1Department of Neurology, The First Affiliated Clinical Hospital of Harbin Medical University, Harbin, People's Republic of China.

Annals of Neurology
|April 30, 2026
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Summary

Interleukin-1 beta (IL-1β) signaling drives Neuromyelitis Optica (NMO) by activating STING in astrocytes. Targeting IL-1β with antisense oligonucleotides (ASOs) shows promise for treating this autoimmune CNS disorder.

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Area of Science:

  • Neuroimmunology
  • Autoimmune diseases
  • Central nervous system (CNS) inflammation

Background:

  • Neuromyelitis Optica (NMO) is a severe autoimmune CNS disorder involving aquaporin-4 antibody (AQP4-IgG)-mediated astrocyte injury.
  • Interleukin-1 beta (IL-1β) signaling exacerbates astrocyte damage and CNS inflammation in NMO.
  • Astrocyte-intrinsic mechanisms linking IL-1β to downstream pathways like STING activation are not well understood.

Purpose of the Study:

  • Elucidate the astrocyte-intrinsic IL-1β-IL-1R STING signaling axis in NMO pathogenesis.
  • Evaluate the therapeutic potential of IL-1β-targeting antisense oligonucleotides (ASOs) for NMO.

Main Methods:

  • Utilized in vitro primary astrocytes, ex vivo organotypic cerebellar slices, and in vivo NMO mouse models.
  • Investigated the IL-1β-IL-1R STING axis using IL-1β neutralizing antibody, astrocyte-specific IL-1β knockout, IL-1R inhibitor Anakinra, and STING genetic ablation.
  • Performed behavioral, histopathological, and molecular analyses to assess NMO pathology.

Main Results:

  • IL-1β signaling via IL-1R induces STING-dependent pro-inflammatory cytokine production in astrocytes.
  • This inflammatory cascade was suppressed by anakinra or STING genetic ablation.
  • Therapeutic IL-1β ASO administration reduced IL-1β expression, preserved AQP4 and myelin, and improved functional outcomes.

Conclusions:

  • The IL-1β-IL-1R STING signaling axis is a key driver of NMO pathogenesis.
  • IL-1β ASO therapy represents a promising disease-modifying strategy for NMO.