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However, the role and mechanism of TIA1\u2010mediated SGs in experimental autoimmune encephalomyelitis (EAE) remain unclear. In this study, upregulation of TIA1, its translocation from the nucleus to the cytoplasm, and co\u2010localization with G3BP1 (a marker of SGs) are observed in the spinal cord neurons of EAE mice. Deletion of TIA1 in the CNS alleviates neuroinflammation, suppresses demyelination and axonal damage, and reduces neuronal loss in EAE mice. Furthermore, alleviation of autophagy dysfunction and reduction of chronic persistent SGs are observed in\n                    <jats:italic>Tia1<\/jats:italic>\n                    <jats:sup>Nestin<\/jats:sup>\n                    \u2010CKO EAE mice. Mechanistically, IL\u201031RA levels are decreased in\n                    <jats:italic>Tia1<\/jats:italic>\n                    <jats:sup>Nestin<\/jats:sup>\n                    \u2010CKO EAE mice, which inhibit the downstream PI3K\/AKT signaling pathway associated with IL\u201031RA, thereby enhancing autophagy and suppressing the NF\u2010\u03baB signaling pathway, further alleviating EAE symptoms. Knockdown of TIA1 in primary neurons and N2a cells treated with sodium arsenite also reduces the formation of SGs. These findings reveal an unrecognized role of TIA1\u2010mediated SGs in promoting neuroinflammation and demyelination, offering novel therapeutic targets for MS.\n                  <\/jats:p>","DOI":"10.1002\/advs.202409086","type":"journal-article","created":{"date-parts":[[2025,1,13]],"date-time":"2025-01-13T14:45:02Z","timestamp":1736779502000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":12,"title":["TIA1\u2010Mediated Stress Granules Promote the Neuroinflammation and Demyelination in Experimental Autoimmune Encephalomyelitis through Upregulating IL\u201031RA Signaling"],"prefix":"10.1002","volume":"12","author":[{"given":"Xin","family":"Hua","sequence":"first","affiliation":[{"name":"Department of Neurology The First Affiliated Hospital of Wenzhou Medical University  Wenzhou Zhejiang 325000 China"},{"name":"Department of Neurology Xuanwu Hospital Capital Medical University National Center for Neurological Disorders  Beijing 100053 China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lingting","family":"Jin","sequence":"additional","affiliation":[{"name":"School of Basic Medical Sciences Wenzhou Medical University  Wenzhou Zhejiang 325000 China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zheyu","family":"Fang","sequence":"additional","affiliation":[{"name":"Department of Neurology The First Affiliated Hospital of Wenzhou Medical University  Wenzhou Zhejiang 325000 China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yiyun","family":"Weng","sequence":"additional","affiliation":[{"name":"Department of Neurology The First Affiliated Hospital of Wenzhou Medical University  Wenzhou Zhejiang 325000 China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuan","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Neurology The First Affiliated Hospital of Wenzhou Medical University  Wenzhou Zhejiang 325000 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