Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/11173
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dc.contributor.authorTestro, Adam G-
dc.contributor.authorVisvanathan, Kumar-
dc.contributor.authorSkinner, Narelle-
dc.contributor.authorMarkovska, Vesna-
dc.contributor.authorCrowley, Peter-
dc.contributor.authorAngus, Peter W-
dc.contributor.authorGow, Paul J-
dc.date.accessioned2015-05-16T00:45:39Z
dc.date.available2015-05-16T00:45:39Z
dc.date.issued2011-01-01-
dc.identifier.citationJournal of Gastroenterology and Hepatology; 26(1): 155-63en_US
dc.identifier.otherPUBMEDen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/11173en
dc.description.abstractToll-like receptor (TLR) signaling is a crucial step in initiating adaptive immune responses. In addition to recognizing endotoxin, TLR4 also recognizes endogenous ligands ('damage-associated structures'), which are released into the circulation in the peri-transplantation period. TLR2 to a lesser extent also recognizes these endogenous ligands. Multiple studies involving solid organ transplants demonstrate a clear association between TLR4 and allograft rejection. In the present study we assessed whether an association exists between TLR4 and TLR2-dependent responses and acute liver allograft rejection.The sample included 26 liver transplant recipients. Blood was taken pre-transplant and at multiple points over the first 14 days post-transplant. Monocytes were stimulated with TLR4 and TLR2 ligands, lipopolysaccharide and Pam-3-Cys, respectively. Monocyte TLR expression was determined using flow cytometry; enzyme-linked immunosorbent assays measured tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) production.Nine (34.6%) patients experienced rejection. No differences existed in age, sex, disease or immunosuppression between rejectors and non-rejectors. Baseline TLR4 expression was significantly higher in rejectors (1.36 vs 1.02, P=0.01). There was no difference in TLR2 expression. In rejectors, baseline TLR4- and TLR2-dependent production of TNF-α and IL-6 was also significantly increased. Post-transplant, the two groups differed with regard to TLR4-dependent TNF-α production, with rejectors demonstrating progressive downregulation over the first week.Prior to liver transplantation, patients who subsequently experience rejection demonstrate robust TLR4-dependent immune responses, which are not seen in those who do not reject. This supports the theory that damage-associated structures signaling through TLR4 may be responsible for the early activation of alloimmune T-cells, favoring allograft rejection.en_US
dc.language.isoenen
dc.subject.otherAcute Diseaseen
dc.subject.otherAdulten
dc.subject.otherAntigens, CD14.metabolismen
dc.subject.otherCells, Cultureden
dc.subject.otherCysteine.analogs & derivatives.pharmacologyen
dc.subject.otherEnzyme-Linked Immunosorbent Assayen
dc.subject.otherFemaleen
dc.subject.otherFlow Cytometryen
dc.subject.otherGraft Rejection.immunologyen
dc.subject.otherHumansen
dc.subject.otherImmunity, Innate.drug effectsen
dc.subject.otherInterleukin-6.metabolismen
dc.subject.otherLipopolysaccharides.pharmacologyen
dc.subject.otherLipoproteins.pharmacologyen
dc.subject.otherLiver Transplantation.immunologyen
dc.subject.otherMaleen
dc.subject.otherMiddle Ageden
dc.subject.otherMonocytes.drug effects.immunologyen
dc.subject.otherPilot Projectsen
dc.subject.otherProspective Studiesen
dc.subject.otherSignal Transduction.drug effectsen
dc.subject.otherTime Factorsen
dc.subject.otherToll-Like Receptor 2.agonists.metabolismen
dc.subject.otherToll-Like Receptor 4.agonists.metabolismen
dc.subject.otherTransplantation, Homologousen
dc.subject.otherTumor Necrosis Factor-alpha.metabolismen
dc.subject.otherUp-Regulationen
dc.subject.otherVictoriaen
dc.titleAcute allograft rejection in human liver transplant recipients is associated with signaling through toll-like receptor 4.en_US
dc.typeJournal Articleen_US
dc.identifier.journaltitleJournal of Gastroenterology and Hepatologyen_US
dc.identifier.affiliationGeneral Medicineen_US
dc.identifier.doi10.1111/j.1440-1746.2010.06324.xen_US
dc.description.pages155-63en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/21175809en
dc.type.contentTexten_US
dc.type.austinJournal Articleen
local.name.researcherAngus, Peter W
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.fulltextNo Fulltext-
item.grantfulltextnone-
item.languageiso639-1en-
item.openairetypeJournal Article-
crisitem.author.deptVictorian Liver Transplant Unit-
crisitem.author.deptGastroenterology and Hepatology-
crisitem.author.deptVictorian Liver Transplant Unit-
crisitem.author.deptGastroenterology and Hepatology-
crisitem.author.deptVictorian Liver Transplant Unit-
crisitem.author.deptGastroenterology and Hepatology-
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