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10.1155/2015/145305 http://scihub22266oqcxt.onion/10.1155/2015/145305 C4584235!4584235 !26451077     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26451077 &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 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\26451077 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Mediators+Inflamm 2015 ; 2015 (ä): 145305 Nephropedia Template TP {{tp|p=26451077 |t=2015. MiR-146b Mediates Endotoxin Tolerance in Human Phagocytes |pdf=|usr=}}{{26451077 }} gab.com Text MiR-146b Mediates Endotoxin Tolerance in Human Phagocytes JO: Mediators Inflamm http://www.kidney.de/pget.php?&tw=1&pmid=26451077 #FOAvip A proper regulation of the innate immune response is fundamental to keep the immune system in check and avoid a chronic status of inflammation. As they act as negative modulators of TLR signaling pathways, miRNAs have been recently involved in the control of the inflammatory response. However, their role in the context of endotoxin tolerance is just beginning to be explored. We here show that miR-146b is upregulated in human monocytes tolerized by LPS, IL-10, or TGF? priming and demonstrate that its transcription is driven by STAT3 and RUNX3, key factors downstream of IL-10 and TGF? signaling. Our study also found that IFN?, known to revert LPS tolerant state, inhibits miR-146b expression. Finally, we provide evidence that miR-146b levels have a profound effect on the tolerant state, thus candidating miR-146b as a molecular mediator of endotoxin tolerance. Twit Text FOAVip MiR-146b Mediates Endotoxin Tolerance in Human Phagocytes ????Mediators Inflamm http://www.kidney.de/pget.php?&tw=1&pmid=26451077 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26451077 #FOAvip English Wikipedia <ref>{{Cite pmid|26451077 }}</ref> MiR-146b Mediates Endotoxin Tolerance in Human Phagocytes #MMPMID26451077 Renzi TA ; Rubino M ; Gornati L ; Garlanda C ; Locati M ; Curtale G Mediators Inflamm 2015[]; 2015 (ä): 145305 PMID26451077 show ga A proper regulation of the innate immune response is fundamental to keep the immune system in check and avoid a chronic status of inflammation. As they act as negative modulators of TLR signaling pathways, miRNAs have been recently involved in the control of the inflammatory response. However, their role in the context of endotoxin tolerance is just beginning to be explored. We here show that miR-146b is upregulated in human monocytes tolerized by LPS, IL-10, or TGF? priming and demonstrate that its transcription is driven by STAT3 and RUNX3, key factors downstream of IL-10 and TGF? signaling. Our study also found that IFN?, known to revert LPS tolerant state, inhibits miR-146b expression. Finally, we provide evidence that miR-146b levels have a profound effect on the tolerant state, thus candidating miR-146b as a molecular mediator of endotoxin tolerance. |Cell Line [MESH] |Cells, Cultured [MESH] |Chromatin Immunoprecipitation [MESH] |Endotoxins/*pharmacology [MESH] |Enzyme-Linked Immunosorbent Assay [MESH] |Humans [MESH] |Immunoprecipitation [MESH] |Interleukin-10/pharmacology [MESH] |MicroRNAs/genetics/*metabolism [MESH] |Monocytes/drug effects/metabolism [MESH] |Phagocytes/*drug effects/*metabolism [MESH]MiR-146b Mediates Endotoxin Tolerance in Human Phagocytes (epmc).pdf DeepDyve Pubget Overpricing