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dc.contributor.authorAregay, Amare
dc.contributor.authorEngel, Bastian
dc.contributor.authorPort, Kerstin
dc.contributor.authorVondran, Florian W R
dc.contributor.authorBremer, Birgit
dc.contributor.authorNiehaus, Christian
dc.contributor.authorKhera, Tanvi
dc.contributor.authorRichter, Nicolas
dc.contributor.authorJaeckel, Elmar
dc.contributor.authorCornberg, Markus
dc.contributor.authorTaubert, Richard
dc.contributor.authorWedemeyer, Heiner
dc.date.accessioned2021-07-21T14:20:54Z
dc.date.available2021-07-21T14:20:54Z
dc.date.issued2021-02-28
dc.identifier.citationLiver Transpl. 2021 Jun;27(6):887-899. doi: 10.1002/lt.26031.en_US
dc.identifier.pmid33641215
dc.identifier.doi10.1002/lt.26031
dc.identifier.urihttp://hdl.handle.net/10033/622949
dc.description.abstractRecurrence or de novo infection of hepatitis C virus (HCV) after liver transplantation (LT) has been associated with progressive graft hepatitis that can be improved by treatment with novel direct-acting antivirals. Cases of rejection episodes have been described during and after HCV treatment. The evolution of innate and adaptive immune response during and after cure of HCV LT is unknown. We studied 74 protein biomarkers in the plasma of LT patients receiving antiviral therapy. In addition, deep immune phenotyping of both the myeloid and lymphoid immune cell subsets in peripheral blood mononuclear cells was performed. We found that LT patients with active HCV infection displayed distinct alterations of inflammatory protein biomarkers, such as C-X-Cmotif chemokine 10 (CXCL10), caspase 8, C-C motif chemokine 20 (CCL20), CCL19, interferon γ, CUB domain-containing protein 1 (CDCP1), interleukin (IL)-18R1, CXCL11, CCL3, IL8, IL12B, tumor necrosis factor-beta, CXCL6, osteoprotegerin, IL10, fms-related tyrosine kinase 3 ligand, hepatocyte growth factor, urokinase-type plasminogen activator, neurotrophin-3, CCL4, IL6, tumornecrosis factor receptor superfamily member 9, programmed death ligand 1, IL18, and monocyte chemotactic protein 1, and enrichment of peripheral immune cell subsets unlike patients without HCV infection who received transplants. Interestingly, patients who cleared HCV after LT did not normalize the altered inflammatory milieu nor did the peripheral immune cell subsets normalize to what would be seen in the absence of HCV recurrence. Overall, these data indicate that HCV-specific imprints on inflammatory analytes and immune cell subsets after LT are not completely normalized by therapy-induced HCV elimination. This is in line with the clinical observation that cure of HCV after LT did not trigger rejection episodes in many patients.en_US
dc.language.isoenen_US
dc.publisherWileyen_US
dc.rightsAttribution 4.0 International*
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.titleDistinct Immune Imprints of Post-Liver Transplantation Hepatitis C Persist Despite Viral Clearance.en_US
dc.typeArticleen_US
dc.identifier.eissn1527-6473
dc.contributor.departmentCiiM, Zentrum für individualisierte Infektionsmedizin, Feodor-Lynen-Str.7, 30625 Hannover.en_US
dc.identifier.journalLiver transplantation : official publication of the American Association for the Study of Liver Diseases and the International Liver Transplantation Societyen_US
dc.source.volume27
dc.source.issue6
dc.source.beginpage887
dc.source.endpage899
refterms.dateFOA2021-07-21T14:20:54Z
dc.source.journaltitleLiver transplantation : official publication of the American Association for the Study of Liver Diseases and the International Liver Transplantation Society
dc.source.countryUnited States


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Attribution 4.0 International
Except where otherwise noted, this item's license is described as Attribution 4.0 International