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10.1002/eji.201546080 http://scihub22266oqcxt.onion/10.1002/eji.201546080 C5071700!5071700 !26970349     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26970349 &cmd=llinks): Failed to open stream: HTTP request failed! 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Cardiomyocytes display low mitochondrial priming and are highly resistant toward cytotoxic T-cell killing |pdf=|usr=}}{{26970349 }} gab.com Text Cardiomyocytes display low mitochondrial priming and are highly resistant toward cytotoxic T-cell killing JO: Eur J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=26970349 #FOAvip Following heart transplantation, alloimmune responses can cause graft rejection by damaging donor vascular and parenchymal cells. However, it remains unclear whether cardiomyocytes are also directly killed by immune cells. Here, we used two-photon microscopy to investigate how graft-specific effector CD8(+) T cells interact with cardiomyocytes in a mouse heart transplantation model. Surprisingly, we observed that CD8(+) T cells are completely impaired in killing cardiomyocytes. Even after virus-mediated preactivation, antigen-specific CD8(+) T cells largely fail to lyse these cells although both cell types engage in dynamic interactions. Furthermore, we established a two-photon microscopy-based assay using intact myocardium to determine the susceptibility of cardiomyocytes to undergo apoptosis. This feature, also known as mitochondrial priming reveals an unexpected weak predisposition of cardiomyocytes to undergo apoptosis in situ. These observations together with the early exhaustion phenotype of graft-infiltrating specific T cells provide an explanation why cardiomyocytes are largely protected from direct CD8(+) T-cell-mediated killing. Twit Text FOAVip Cardiomyocytes display low mitochondrial priming and are highly resistant toward cytotoxic T-cell killing ????Eur J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=26970349 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26970349 #FOAvip English Wikipedia <ref>{{Cite pmid|26970349 }}</ref> Cardiomyocytes display low mitochondrial priming and are highly resistant toward cytotoxic T-cell killing #MMPMID26970349 Zheng X ; Halle S ; Yu K ; Mishra P ; Scherr M ; Pietzsch S ; Willenzon S ; Janssen A ; Boelter J ; Hilfiker-Kleiner D ; Eder M ; Förster R Eur J Immunol 2016[Jun]; 46 (6 ): 1415-26 PMID26970349 show ga Following heart transplantation, alloimmune responses can cause graft rejection by damaging donor vascular and parenchymal cells. However, it remains unclear whether cardiomyocytes are also directly killed by immune cells. Here, we used two-photon microscopy to investigate how graft-specific effector CD8(+) T cells interact with cardiomyocytes in a mouse heart transplantation model. Surprisingly, we observed that CD8(+) T cells are completely impaired in killing cardiomyocytes. Even after virus-mediated preactivation, antigen-specific CD8(+) T cells largely fail to lyse these cells although both cell types engage in dynamic interactions. Furthermore, we established a two-photon microscopy-based assay using intact myocardium to determine the susceptibility of cardiomyocytes to undergo apoptosis. This feature, also known as mitochondrial priming reveals an unexpected weak predisposition of cardiomyocytes to undergo apoptosis in situ. These observations together with the early exhaustion phenotype of graft-infiltrating specific T cells provide an explanation why cardiomyocytes are largely protected from direct CD8(+) T-cell-mediated killing. äCardiomyocytes display low mitochondrial priming and are highly resist(epmc).pdf DeepDyve Pubget Overpricing