{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,22]],"date-time":"2026-09-22T13:06:49Z","timestamp":1790082409968,"version":"4.0.1"},"reference-count":84,"publisher":"Oxford University Press (OUP)","issue":"8","license":[{"start":{"date-parts":[[2014,10,1]],"date-time":"2014-10-01T00:00:00Z","timestamp":1412121600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2014,10,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Immune cell entry into the virally infected CNS is vital for promoting viral clearance yet may contribute to neuropathology if not rigorously regulated. We previously showed that signaling through IL-1R1 is critical for effector T cell reactivation and virologic control within the CNS during murine West Nile virus (WNV) encephalitis. WNV-infected IL-1R1\u2212\/\u2212 mice also display increased parenchymal penetration of CD8+ T cells despite lack of CD4-mediated full activation, suggesting dysregulation of molecular components of CNS immune privilege. In this study, we show that IL-1 signaling regulates the CNS entry of virus-specific lymphocytes, promoting protective immune responses to CNS viral infections that limit immunopathology. Analysis of blood\u2013brain barrier function in the WNV-infected IL-1R1\u2212\/\u2212 mice revealed no alterations in permeability. However, parenchymal proinflammatory chemokine expression, including CCL2, CCL5, and CXCL10, was significantly upregulated, whereas microvasculature CXCL12 expression was significantly decreased in the absence of IL-1 signaling. We show that during WNV infection, CD11b+CD45hi infiltrating cells (macrophages) are the primary producers of IL-1\u03b2 within the CNS and, through the use of an in vitro blood\u2013brain barrier model, that IL-1\u03b2 promotes CXCR4-mediated T cell adhesion to brain microvasculature endothelial cells. Of interest, IFN\u03b3+ and CD69+ WNV-primed T cells were able to overcome CXCL12-mediated adhesion via downregulation of CXCR4. These data indicate that infiltrating IL-1\u03b2\u2013producing leukocytes contribute to cellular interactions at endothelial barriers that impart protective CNS inflammation by regulating the parenchymal entry of CXCR4+ virus-specific T cells during WNV infection.<\/jats:p>","DOI":"10.4049\/jimmunol.1401192","type":"journal-article","created":{"date-parts":[[2014,9,9]],"date-time":"2014-09-09T00:36:46Z","timestamp":1410223006000},"page":"4095-4106","source":"Crossref","is-referenced-by-count":59,"title":["IL-1R1 Signaling Regulates CXCL12-Mediated T Cell Localization and Fate within the Central Nervous System during West Nile Virus Encephalitis"],"prefix":"10.1093","volume":"193","author":[{"given":"Douglas M","family":"Durrant","sequence":"first","affiliation":[{"name":"Department of Medicine, Washington University School of Medicine , St. Louis, MO 63110"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brian P","family":"Daniels","sequence":"additional","affiliation":[{"name":"Department of Medicine, Washington University School of Medicine , St. Louis, MO 63110"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robyn S","family":"Klein","sequence":"additional","affiliation":[{"name":"Department of Medicine, Washington University School of Medicine , St. Louis, MO 63110"},{"name":"Department of Anatomy and Neurobiology, Washington University School of Medicine , St. Louis, MO 63110"},{"name":"Department of Pathology and Immunology, Washington University School of Medicine , St. Louis, MO 63110"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2014,10,15]]},"reference":[{"key":"2025030707393010000_r1","doi-asserted-by":"crossref","first-page":"4","DOI":"10.1186\/2045-8118-8-4","article-title":"Fluids and barriers of the CNS establish immune privilege by confining immune surveillance to a two-walled castle moat surrounding the CNS castle","volume":"8","author":"Engelhardt","year":"2011","journal-title":"Fluids Barriers CNS"},{"key":"2025030707393010000_r2","doi-asserted-by":"crossref","first-page":"799","DOI":"10.2353\/ajpath.2008.070918","article-title":"Pathological expression of CXCL12 at the blood-brain barrier correlates with severity of multiple sclerosis","volume":"172","author":"McCandless","year":"2008","journal-title":"Am. 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