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In this study, we first observed that knockdown of neuropilin-1 (NRP1), a co-receptor of several structurally diverse ligands, suppressed interferon-\u03b3 (IFN\u03b3)-induced C-X-C motif chemokine 10 expression and activation of STAT1 in brain microvascular endothelial cells in a Rac1-dependent manner. Moreover, endothelial-specific NRP1-knockout mice, VECadherin-Cre-ERT2\/NRP1flox\/flox mice, showed attenuated disease progression during experimental autoimmune encephalomyelitis, a mouse neuroinflammatory disease model. Detailed analysis utilizing histological staining, quantitative PCR, flow cytometry and magnetic resonance imaging demonstrated that deletion of endothelial NRP1 suppressed neuron demyelination, altered lymphocyte infiltration, preserved BBB function and decreased activation of the STAT1\u2013CXCL10 pathway. Furthermore, increased expression of NRP1 was observed in endothelial cells of acute multiple sclerosis lesions. Our data identify a new molecular mechanism of brain microvascular endothelial inflammatory response through NRP1\u2013IFN\u03b3 crosstalk that could be a potential target for intervention of endothelial cell dysfunction in neuroinflammatory diseases.<\/jats:p>","DOI":"10.1242\/jcs.190702","type":"journal-article","created":{"date-parts":[[2016,9,2]],"date-time":"2016-09-02T22:09:05Z","timestamp":1472854145000},"page":"3911-3921","source":"Crossref","is-referenced-by-count":46,"title":["Neuropilin-1 modulates interferon-\u03b3-stimulated signaling in brain microvascular endothelial cells"],"prefix":"10.1242","volume":"129","author":[{"given":"Ying","family":"Wang","sequence":"first","affiliation":[{"name":"Mayo Clinic 1 Department of Biochemistry and Molecular Biology , , Jacksonville, FL 32224 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