{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,5,2]],"date-time":"2025-05-02T00:29:41Z","timestamp":1746145781872},"reference-count":46,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2012,6,1]],"date-time":"2012-06-01T00:00:00Z","timestamp":1338508800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Transplant Infectious Dis"],"published-print":{"date-parts":[[2012,10]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:label \/><jats:p>The development of liver and graft disease is suspected to be affected by genetic diversity. Mannose\u2010binding lectin\u20102 (<jats:styled-content style=\"fixed-case\">MBL<\/jats:styled-content>\u20102) is an important immunomodulatory factor that is involved in complement activation. The aim of our study was to elucidate the role of <jats:styled-content style=\"fixed-case\">MBL<\/jats:styled-content>\u20102 genotypes after liver transplantation (<jats:styled-content style=\"fixed-case\">LT<\/jats:styled-content>) for hepatitis C virus (<jats:styled-content style=\"fixed-case\">HCV<\/jats:styled-content>)\u2010induced liver disease regarding the incidence of acute cellular rejection (<jats:styled-content style=\"fixed-case\">ACR<\/jats:styled-content>), graft inflammation, fibrosis development, and antiviral treatment response.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>A group of 149 patients who underwent <jats:styled-content style=\"fixed-case\">LT<\/jats:styled-content> for <jats:styled-content style=\"fixed-case\">HCV<\/jats:styled-content>\u2010induced liver disease were genotyped for <jats:styled-content style=\"fixed-case\">MBL<\/jats:styled-content>\u20102 (rs7096206; G\/C) by TaqMan genotyping assay. We evaluated 518 post\u2010<jats:styled-content style=\"fixed-case\">LT<\/jats:styled-content> protocol biopsies and at least 98 urgent liver biopsies regarding graft fibrosis stages, inflammation grades, and evidence for rejection within <jats:styled-content style=\"fixed-case\">MBL<\/jats:styled-content>\u20102 genotype groups.<\/jats:p><\/jats:sec><jats:sec><jats:title>Result<\/jats:title><jats:p>No association of <jats:styled-content style=\"fixed-case\">MBL<\/jats:styled-content>\u20102 polymorphisms was observed regarding inflammation, fibrosis, and antiviral treatment outcome. However, the C allele of the <jats:styled-content style=\"fixed-case\">MBL<\/jats:styled-content>\u20102 gene (<jats:italic>P<\/jats:italic>\u00a0=\u00a00.001) and gender compatibility (<jats:italic>P<\/jats:italic>\u00a0=\u00a00.012) were factors significantly associated with the incidence of <jats:styled-content style=\"fixed-case\">ACR<\/jats:styled-content>.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p><jats:styled-content style=\"fixed-case\">MBL<\/jats:styled-content>\u20102 polymorphisms and gender are involved in the development of <jats:styled-content style=\"fixed-case\">ACR<\/jats:styled-content> after <jats:styled-content style=\"fixed-case\">LT<\/jats:styled-content>. <jats:styled-content style=\"fixed-case\">CC<\/jats:styled-content> genotype and gender match may be regarded as risk factors for <jats:styled-content style=\"fixed-case\">ACR<\/jats:styled-content> in <jats:styled-content style=\"fixed-case\">HCV<\/jats:styled-content>\u2010positive graft recipients. Further studies are needed to confirm and verify this observation in non\u2010<jats:styled-content style=\"fixed-case\">HCV<\/jats:styled-content> groups as well.<\/jats:p><\/jats:sec>","DOI":"10.1111\/j.1399-3062.2012.00747.x","type":"journal-article","created":{"date-parts":[[2012,6,1]],"date-time":"2012-06-01T08:51:38Z","timestamp":1338540698000},"page":"488-495","source":"Crossref","is-referenced-by-count":10,"title":["Role of mannose\u2010binding lectin\u20102 polymorphism in the development of acute cellular rejection after transplantation for hepatitis <scp>C<\/scp> virus\u2010induced liver disease"],"prefix":"10.1111","volume":"14","author":[{"given":"D.","family":"Eurich","sequence":"first","affiliation":[{"name":"Department of General, Visceral and Transplantation Surgery Charit\u00e9 Campus Virchow Berlin Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"S.","family":"Boas\u2010Knoop","sequence":"additional","affiliation":[{"name":"Department of 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