{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"institution":[{"name":"bioRxiv"}],"indexed":{"date-parts":[[2026,7,30]],"date-time":"2026-07-30T12:12:25Z","timestamp":1785413545894,"version":"3.56.0"},"posted":{"date-parts":[[2026,1,20]]},"group-title":"Neuroscience","reference-count":40,"publisher":"openRxiv","license":[{"start":{"date-parts":[[2026,1,20]],"date-time":"2026-01-20T00:00:00Z","timestamp":1768867200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"funder":[{"award":["R35GM146890"],"award-info":[{"award-number":["R35GM146890"]}],"id":[{"id":"https:\/\/ror.org\/001d55x84","id-type":"ROR","asserted-by":"publisher"}]},{"award":["R03NS144870"],"award-info":[{"award-number":["R03NS144870"]}],"id":[{"id":"https:\/\/ror.org\/001d55x84","id-type":"ROR","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"accepted":{"date-parts":[[2026,1,26]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                <jats:p>\n                  Nerve Injury-Induced Protein 1 (Ninjurin-1) is an adhesion molecule implicated in inflammation and tissue injury, yet its role in neuroinflammatory diseases such as multiple sclerosis (MS) remains poorly defined. Here, we identify Ninjurin-1 as a key mediator of immune activation and CNS infiltration in relapsing-remitting experimental autoimmune encephalomyelitis (RR-EAE), a model of relapsing-remitting MS (RRMS). Using flow cytometry, gene-expression profiling, and\n                  <jats:italic>in vivo<\/jats:italic>\n                  peptide blockade, we show that Ninjurin-1 is markedly upregulated on CNS-infiltrating myeloid cells during disease progression. Ninjurin-1\u207a myeloid cells display a dual function, as both an adhesion molecule and a marker of inflammatory activation, characterized by increased antigen presentation, cytokine production, and transcriptional enrichment for genes regulating adhesion, migration, and innate immune signaling. Importantly, therapeutic blockade of Ninjurin-1 significantly reduced clinical severity, CNS immune infiltration, and demyelination in RR-EAE. These findings uncover a previously unrecognized role for Ninjurin-1 in myeloid-driven neuroinflammation and highlight its potential as a therapeutic target for relapsing-remitting MS.\n                <\/jats:p>","DOI":"10.64898\/2026.01.16.699993","type":"posted-content","created":{"date-parts":[[2026,1,21]],"date-time":"2026-01-21T03:35:14Z","timestamp":1768966514000},"source":"Crossref","is-referenced-by-count":0,"title":["Dual Role of Ninjurin-1 in Myeloid Cell Adhesion and Inflammation in Relapse-Remitting EAE"],"prefix":"10.64898","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0591-7654","authenticated-orcid":false,"given":"Coleen","family":"Thompson","sequence":"first","affiliation":[{"name":"Department of Molecular and Cellular Biology, College of Medicine, University of Cincinnati, Cincinnati, OH USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alex","family":"Annett","sequence":"additional","affiliation":[{"name":"Department of Molecular and Cellular 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