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Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Science 2015 ; 349 (6245): 316-20 Nephropedia Template TP
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Neutrophil extracellular traps license macrophages and Th17 cells for cytokine production in atherosclerosis #MMPMID26185250
Warnatsch A; Ioannou M; Wang Q; Papayannopoulos V
Science 2015[Jul]; 349 (6245): 316-20 PMID26185250show ga
Secretion of the cytokine interleukin-1? (IL-1?) by macrophages, a major driver of pathogenesis in atherosclerosis, requires two steps. First, priming signals promote transcription of immature IL-1? and then, endogenous ?danger? signals activate innate immune signaling complexes called inflammasomes, to process IL-1? processing for secretion. While cholesterol crystals act as danger signals in atherosclerosis, what primes IL-1? transcription remains elusive. Using a murine model of atherosclerosis, we show 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 Th-17 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.