{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,2]],"date-time":"2025-11-02T16:17:11Z","timestamp":1762100231863,"version":"3.30.0"},"reference-count":55,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"3","license":[{"start":{"date-parts":[[2015,9,1]],"date-time":"2015-09-01T00:00:00Z","timestamp":1441065600000},"content-version":"tdm","delay-in-days":6028,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[1999,3]]},"abstract":"<jats:sec>\n            <jats:title\/>\n            <jats:p>Intercellular adhesion molecule\u20131(ICAM\u20131) is expressed abnormally on the bile duct epithelium during the course of primary biliary cirrhosis (PBC), but the importance of ICAM\u20131 and its lymphocyte function\u2013associated antigen\u20131 (LFA\u20131) receptor during the course of nonsuppurative destructive cholangitis (NSDC) has not been defined. To address this question, we defined the relationship between ICAM\u20131 on the intrahepatic bile duct epithelium and the evolution of NSDC lesions in a mouse graft\u2013versus\u2013host disease (GVHD) model. We also determined the effects of anti-ICAM\u20131 and anti-LFA\u20131 treatments on NSDC, intrahepatic lymphokine production, and the homing of lymphocytes to the livers of GVHD mice. ICAM\u20131 was initially detected on the bile duct epithelium and portal vein endothelium on day 7 of GVHD. There was a significant positive correlation between the intensity of ICAM\u20131 staining and histological bile duct damage (<jats:italic toggle=\"yes\">r<\/jats:italic> = .58, <jats:italic toggle=\"yes\">P<\/jats:italic> &lt; .05) between day 3 and 28. Treatment with anti-ICAM\u20131 (but not anti-LFA\u20131) decreased both the mean grades of portal inflammation (<jats:italic toggle=\"yes\">P<\/jats:italic> = .003) and NSDC (<jats:italic toggle=\"yes\">P<\/jats:italic> = .002) lesions compared with control immunoglobulin G (IgG) treatments. Combined treatment with anti-ICAM\u20131 and anti-LFA\u20131 caused a further decrease in the amount of portal inflammation and bile duct damage compared with anti-ICAM\u20131, alone (<jats:italic toggle=\"yes\">P<\/jats:italic> = .02). Anti-ICAM\u20131 treatment also decreased both the percentage of T cells and the production of interleukin\u20132 (IL\u20132) and IL\u201312 in the liver (<jats:italic toggle=\"yes\">P<\/jats:italic> &lt; .01), but had no effect on IL\u20134, IL\u201310, and interferon gamma. Neither anti-ICAM\u20131 nor anti-LFA\u20131 prevented lymphocytes from homing to the liver. These results indicate that both ICAM\u20131 and LFA\u20131 are important to the pathogenesis of NSDC<\/jats:p>\n          <\/jats:sec>","DOI":"10.1002\/hep.510290350","type":"journal-article","created":{"date-parts":[[2004,7,28]],"date-time":"2004-07-28T07:25:38Z","timestamp":1090999538000},"page":"766-776","update-policy":"http:\/\/dx.doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":21,"title":["Role of Intercellular Adhesion Molecule\u20131 and Lymphocyte Function-Associated Antigen\u20131 During Nonsuppurative Destructive Cholangitis in A Mouse Graft\u2013Versus\u2013Host Disease Model"],"prefix":"10.1097","volume":"29","author":[{"given":"Charles 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