{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T01:54:37Z","timestamp":1790819677347,"version":"4.1.0"},"reference-count":95,"publisher":"Wiley","issue":"41","license":[{"start":{"date-parts":[[2026,4,29]],"date-time":"2026-04-29T00:00:00Z","timestamp":1777420800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,4,29]],"date-time":"2026-04-29T00:00:00Z","timestamp":1777420800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["advanced.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Advanced Science"],"published-print":{"date-parts":[[2026,7]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Neuroinflammation disrupts the blood\u2013brain barrier (BBB) and drives neurological disease, but current in vitro MPS and animal models fail to capture its dynamic, human\u2010specific immune complexity. Here, we introduce a 3D human immune\u2010competent BBB (3D\u2010HIC\u2010BBB) platform that reconstitutes the neurovascular unit (NVU) by integrating primary human brain microvascular endothelial cells, astrocytes, brain vascular pericytes, human microglia, and dopaminergic neurospheroids with embedded transepithelial electrical resistance (TEER) microsensors for continuous functional monitoring. Our platform design enables high\u2010resolution of inflammatory NVU dynamics that are inaccessible to conventional endpoint assays. Using controlled exposure to tumor necrosis factor\u2010\u03b1 (TNF\u2010\u03b1) and lipopolysaccharide (LPS), two distinct triggers of immune responses, we observed stimulus\u2010specific neuroinflammatory responses with distinct temporal and functional signatures with the resistance full width at half maximum (FWHM) for LPS = 15.8\u00a0h and TNF\u2010\u03b1\u00a0\u00a0= 4.3\u00a0h. TNF\u2010\u03b1 exposure elicited a lesser (\u0394345\u00a0\u2126\u00b7cm\n                    <jats:sup>2<\/jats:sup>\n                    ) but faster drop in resistance and largely faster and reversible recovery than LPS, consistent with transient cytokine\u2010driven disruption. In contrast, LPS induced a delayed yet more severe (\u0394560 \u2126\u00b7cm\n                    <jats:sup>2<\/jats:sup>\n                    ) loss. The 3D\u2010HIC\u2010BBB platform distinguishes endotoxin\u2010 from cytokine\u2010driven NVU dysfunction and reveals differences in cytokine profiles. It provides a biologically relevant, predictive model for studying neuroinflammation and evaluating anti\u2010inflammatory therapies.\n                  <\/jats:p>","DOI":"10.1002\/advs.75461","type":"journal-article","created":{"date-parts":[[2026,4,29]],"date-time":"2026-04-29T15:15:08Z","timestamp":1777475708000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Development of a Human 3D Immune\u2010Competent Neurovascular Model Enabling Time\u2010Resolved Monitoring of Neuroinflammatory Dynamics and Neuroimmune Interactions"],"prefix":"10.1002","volume":"13","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8275-1910","authenticated-orcid":false,"given":"Pavlo","family":"Gordiichuk","sequence":"first","affiliation":[{"name":"Triton Systems, Inc.  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