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10.1172/JCI88621 http://scihub22266oqcxt.onion/10.1172/JCI88621 C4922716!4922716 !27322057     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27322057 &cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\27322057 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       J+Clin+Invest 2016 ; 126 (7 ): 2422-4 Nephropedia Template TP {{tp|p=27322057 |t=2016. Micromanaging alloimmunity |pdf=|usr=}}{{27322057 }} gab.com Text Micromanaging alloimmunity JO: J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=27322057 #FOAvip Increasing evidence indicates that microbes have a large influence on immune function. Previous studies have linked pathogenic microorganisms with decreased allograft tolerance and subsequent rejection. In this issue of the JCI, Lei and colleagues demonstrate that commensal organisms also influence the host response to allograft transplantation. Using murine skin and cardiac transplant models, the authors demonstrate that allograft rejection is accelerated in mice with a normal microbiome compared with germ-free animals and antibiotic-treated mice. The increased graft rejection observed in conventional animals was due to enhanced T cell priming and was mediated through type I IFN. Together, these results suggest that altering a patient's microbial community prior to transplant could improve allograft acceptance. Twit Text FOAVip Micromanaging alloimmunity ????J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=27322057 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27322057 #FOAvip English Wikipedia <ref>{{Cite pmid|27322057 }}</ref> Micromanaging alloimmunity #MMPMID27322057 Ford ML J Clin Invest 2016[Jul]; 126 (7 ): 2422-4 PMID27322057 show ga Increasing evidence indicates that microbes have a large influence on immune function. Previous studies have linked pathogenic microorganisms with decreased allograft tolerance and subsequent rejection. In this issue of the JCI, Lei and colleagues demonstrate that commensal organisms also influence the host response to allograft transplantation. Using murine skin and cardiac transplant models, the authors demonstrate that allograft rejection is accelerated in mice with a normal microbiome compared with germ-free animals and antibiotic-treated mice. The increased graft rejection observed in conventional animals was due to enhanced T cell priming and was mediated through type I IFN. Together, these results suggest that altering a patient's microbial community prior to transplant could improve allograft acceptance. |*Heart Transplantation [MESH] |Animals [MESH] |Graft Rejection/*immunology [MESH] |Graft Survival [MESH] |Humans [MESH] |Mice [MESH] |Mice, Inbred BALB C [MESH] |Mice, Inbred C57BL [MESH]Micromanaging alloimmunity (epmc).pdf DeepDyve Pubget Overpricing