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10.1126/science.aaa8064 http://scihub22266oqcxt.onion/10.1126/science.aaa8064 C4854322!4854322 !26185250     free     free     free 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 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 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 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 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\26185250 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Science 2015 ; 349 (6245 ): 316-20 Nephropedia Template TP {{tp|p=26185250 |t=2015. Inflammation Neutrophil extracellular traps license macrophages for cytokine production in atherosclerosis |pdf=|usr=}}{{26185250 }} gab.com Text Inflammation Neutrophil extracellular traps license macrophages for cytokine production in atherosclerosis JO: Science http://www.kidney.de/pget.php?&tw=1&pmid=26185250 #FOAvip Secretion of the cytokine interleukin-1? (IL-1?) by macrophages, a major driver of pathogenesis in atherosclerosis, requires two steps: Priming signals promote transcription of immature IL-1?, and then endogenous "danger" signals activate innate immune signaling complexes called inflammasomes to process IL-1? for secretion. Although cholesterol crystals are known to act as danger signals in atherosclerosis, what primes IL-1? transcription remains elusive. Using a murine model of atherosclerosis, we found that cholesterol crystals acted both as priming and danger signals for IL-1? production. Cholesterol crystals triggered neutrophils to release neutrophil extracellular traps (NETs). NETs primed macrophages for cytokine release, activating T helper 17 (TH17) cells that amplify immune cell recruitment in atherosclerotic plaques. Therefore, danger signals may drive sterile inflammation, such as that seen in atherosclerosis, through their interactions with neutrophils. Twit Text FOAVip Inflammation Neutrophil extracellular traps license macrophages for cytokine production in atherosclerosis ????Science http://www.kidney.de/pget.php?&tw=1&pmid=26185250 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26185250 #FOAvip English Wikipedia <ref>{{Cite pmid|26185250 }}</ref> Inflammation Neutrophil extracellular traps license macrophages for cytokine production in atherosclerosis #MMPMID26185250 Warnatsch A ; Ioannou M ; Wang Q ; Papayannopoulos V Science 2015[Jul]; 349 (6245 ): 316-20 PMID26185250 show ga Secretion of the cytokine interleukin-1? (IL-1?) by macrophages, a major driver of pathogenesis in atherosclerosis, requires two steps: Priming signals promote transcription of immature IL-1?, and then endogenous "danger" signals activate innate immune signaling complexes called inflammasomes to process IL-1? for secretion. Although cholesterol crystals are known to act as danger signals in atherosclerosis, what primes IL-1? transcription remains elusive. Using a murine model of atherosclerosis, we found that cholesterol crystals acted both as priming and danger signals for IL-1? production. Cholesterol crystals triggered neutrophils to release neutrophil extracellular traps (NETs). NETs primed macrophages for cytokine release, activating T helper 17 (TH17) cells that amplify immune cell recruitment in atherosclerotic plaques. Therefore, danger signals may drive sterile inflammation, such as that seen in atherosclerosis, through their interactions with neutrophils. |Animals [MESH] |Apolipoproteins E/genetics [MESH] |Atherosclerosis/*immunology [MESH] |Cells, Cultured [MESH] |Cholesterol/chemistry/immunology [MESH] |Disease Models, Animal [MESH] |Extracellular Traps/*immunology [MESH] |Humans [MESH] |Inflammasomes/immunology [MESH] |Inflammation/immunology [MESH] |Interleukin-1beta/*biosynthesis/genetics [MESH] |Macrophages/*immunology [MESH] |Mice [MESH] |Mice, Mutant Strains [MESH] |Neutrophils/*immunology [MESH] |Signal Transduction [MESH] |Th17 Cells/immunology [MESH]Inflammation Neutrophil extracellular traps license macrophages for c(epmc).pdf DeepDyve Pubget Overpricing