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IL\u20101\u03b2\u2013mediated inflammatory signaling plays a critical role in amplifying astrocyte damage and propagating CNS inflammation in NMO. However, the astrocyte\u2010intrinsic mechanisms linking IL\u20101\u03b2 signaling to downstream pathways, such as STING activation, remain poorly understood. To address this knowledge gap, in this study, we aim to elucidate the astrocyte\u2010intrinsic mechanisms, specifically the IL\u20101\u03b2\u2013IL\u20101R STING signaling axis, that contribute to NMO pathogenesis, and to evaluate the therapeutic potential of IL\u20101\u03b2\u2010targeting antisense oligonucleotides (ASOs).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Using a multi\u2010level experimental system comprising in vitro primary astrocytes, ex vivo organotypic cerebellar slices, and in vivo NMO mouse models, we systematically investigated the critical role of the astrocytic IL\u20101\u03b2\u2013IL\u20101R STING signaling axis in NMO pathogenesis. Utilizing diverse interventions\u2014including an IL\u20101\u03b2\u2013neutralizing antibody, astrocyte\u2010specific IL\u20101\u03b2 knockout, the IL\u20101R inhibitor Anakinra, STING genetic ablation, and IL\u20101\u03b2 ASOs\u2014in conjunction with behavioral, histopathological, and molecular analyses, we comprehensively delineated the impact of this signaling pathway on NMO pathology. These data support the translation of targeted therapeutic strategies.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>IL\u20101\u03b2 signals through the IL\u20101 receptor (IL\u20101R) to induce STING\u2010dependent proinflammatory cytokine production in astrocytes. This inflammatory cascade can be suppressed by the IL\u20101R antagonist anakinra or genetic ablation of STING. Therapeutic administration of lead IL\u20101\u03b2 targeting ASO reduces IL\u20101\u03b2 expression, preserves AQP4 levels and myelin integrity, and improves functional outcomes.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Interpretation<\/jats:title>\n                    <jats:p>The IL\u20101\u03b2\u2013IL\u20101R STING signaling axis is a central contributor to NMO pathogenesis and supports IL\u20101\u03b2 ASO therapy as a promising potential disease\u2010modifying approach. ANN NEUROL 2026;100:487\u2013510<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/ana.78233","type":"journal-article","created":{"date-parts":[[2026,4,30]],"date-time":"2026-04-30T12:49:46Z","timestamp":1777553386000},"page":"487-510","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["The\n                    <scp>IL<\/scp>\n                    \u20101\u03b2\u2010\n                    <scp>STING<\/scp>\n                    Signaling Axis Drives Neuromyelitis Optica Pathogenesis in a Murine Model"],"prefix":"10.1002","volume":"100","author":[{"given":"Siyu","family":"Han","sequence":"first","affiliation":[{"name":"Department of Neurology The First Affiliated Clinical Hospital of Harbin Medical University  Harbin People's Republic of China"},{"name":"Department of Neurobiology School of Basic Medical Sciences, Harbin Medical University  Harbin People's Republic of 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