{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,26]],"date-time":"2026-09-26T05:52:56Z","timestamp":1790401976934,"version":"4.1.0"},"reference-count":69,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2012,8,23]],"date-time":"2012-08-23T00:00:00Z","timestamp":1345680000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal Cellular Physiology"],"published-print":{"date-parts":[[2012,12]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>The mechanisms of hematogenous leukocyte trafficking at the human blood\u2013nerve barrier (BNB) are largely unknown. Intercellular adhesion molecule\u20101 (ICAM\u20101) has been implicated in the pathogenesis of Guillain\u2013Barr\u00e9 syndrome (GBS). We developed a cytokine\u2010activated human in vitro BNB model using primary endoneurial endothelial cells. Endothelial treatment with 10\u2009U\/ml tissue necrosis factor\u2010\u03b1 and 20\u2009U\/ml interferon\u2010\u03b3 resulted in de novo expression of pro\u2010inflammatory chemokines CCL2, CXCL9, CXCL11, and CCL20, with increased expression of CXCL2\u20133, CXCL8, and CXCL10 relative to basal levels. Cytokine treatment induced\/enhanced ICAM\u20101, E\u2010 and P\u2010selectin, vascular cell adhesion molecule\u20101 and the alternatively spliced pro\u2010adhesive fibronectin variant, fibronectin connecting segment\u20101 expression in a time\u2010dependent manner, without alterations in junctional adhesion molecule\u2010A expression. Lymphocytes and monocytes from untreated GBS patients express ICAM\u20101 counterligands, \u03b1<jats:sub>M<\/jats:sub>\u2010 and \u03b1<jats:sub>L<\/jats:sub>\u2010integrin, with differential regulation of \u03b1<jats:sub>M<\/jats:sub>\u2010integrin expression compared to healthy controls. Under flow conditions that mimic capillary hemodynamics in vivo, there was a &gt;3\u2010fold increase in total GBS patient and healthy control mononuclear leukocyte adhesion\/migration at the BNB following cytokine treatment relative to the untreated state. Function neutralizing monoclonal antibodies against human \u03b1<jats:sub>M<\/jats:sub>\u2010integrin (CD11b) and ICAM\u20101 reduced untreated GBS patient mononuclear leukocyte trafficking at the BNB by 59% and 64.2%, respectively. Monoclonal antibodies against \u03b1<jats:sub>L<\/jats:sub>\u2010integrin (CD11a) and human intravenous immunoglobulin reduced total leukocyte adhesion\/migration by 22.8% and 17.6%, respectively. This study demonstrates differential regulation of \u03b1<jats:sub>M<\/jats:sub>\u2010integrin on circulating mononuclear cells in GBS, as well as an important role for \u03b1<jats:sub>M<\/jats:sub>\u2010integrin\u2013ICAM\u20101 interactions in pathogenic GBS patient leukocyte trafficking at the human BNB in vitro. J. Cell. Physiol. 227: 3857\u20133875, 2012. \u00a9 2012 Wiley Periodicals, Inc.<\/jats:p>","DOI":"10.1002\/jcp.24100","type":"journal-article","created":{"date-parts":[[2012,5,2]],"date-time":"2012-05-02T15:09:39Z","timestamp":1335971379000},"page":"3857-3875","source":"Crossref","is-referenced-by-count":36,"title":["\u03b1<sub>M<\/sub>\u03b2<sub>2<\/sub>\u2010integrin\u2010intercellular adhesion molecule\u20101 interactions drive the flow\u2010dependent trafficking of Guillain\u2013Barr\u00e9 syndrome patient derived mononuclear leukocytes at the blood\u2013nerve barrier in vitro"],"prefix":"10.1002","volume":"227","author":[{"given":"Nejla","family":"Yosef","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eroboghene 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