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pubmed-article:21168672pubmed:abstractTextEvidence suggests that injury-induced activation of the recipient's innate immune response determines the outcome of allograft transplantation. The mechanism responsible for the induction of such innate immune response is not clear yet. We hypothesized that in cardiac transplantation settings, the initial myocardial ischemia and postischemia graft reperfusion may release allograft inflammatory factor (AIF) 1, causing Toll-like receptor (TLR)-mediated activation of macrophages and dendritic cells, leading to the production of cytokines and the activation of adaptive alloimmunity. Therefore, our goal was to validate the presence of these biomarkers in the peripheral blood and biopsy specimens of patients presenting allograft rejection.lld:pubmed
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pubmed-article:21168672pubmed:authorpubmed-author:MooreC KCKlld:pubmed
pubmed-article:21168672pubmed:copyrightInfoCopyright © 2010 Elsevier Inc. All rights reserved.lld:pubmed
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pubmed-article:21168672pubmed:volume42lld:pubmed
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pubmed-article:21168672pubmed:articleTitleCardiac allograft rejection correlates with increased expressions of Toll-like receptors 2 and 4 and allograft inflammatory factor 1.lld:pubmed
pubmed-article:21168672pubmed:affiliationDepartment of Surgery, University of Mississippi Medical Center, Jackson, Mississippi 39216-4505, USA. omcdaniel@umc.edulld:pubmed
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