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Nature Research, Nature Immunology, 2(15), p. 152-160, 2013

DOI: 10.1038/ni.2784

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High-density lipoprotein mediates anti-inflammatory reprogramming of macrophages via the transcriptional regulator ATF3

Journal article published in 2013 by Dominic De Nardo, Larisa I. Labzin, Hajime Kono, Reiko Seki, Susanne V. Schmidt, Marc Beyer, Dakang Xu, Sebastian Zimmer, Catharina Lahrmann, Frank A. Schildberg, Johanna Vogelhuber, Michael Kraut, Thomas Ulas, Anja Kerksiek, Wolfgang Krebs and other authors.
This paper is available in a repository.
This paper is available in a repository.

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Abstract

High Density Lipoprotein (HDL) mediates reverse cholesterol transport and it is known to be protective against atherosclerosis. In addition, HDL has potent anti-inflammatory properties that may be critical for protection against other inflammatory diseases. The molecular mechanisms of how HDL can modulate inflammation, particularly in immune cells such as macrophages, remain poorly understood. Here we identify the transcriptional repressor ATF3, as an HDL-inducible target gene in macrophages that down-regulates the expression of Toll-like receptor (TLR)-induced pro-inflammatory cytokines. The protective effects of HDL against TLR-induced inflammation were fully dependent on ATF3 in vitro and in vivo. Our findings may explain the broad anti-inflammatory and metabolic actions of HDL and provide the basis for predicting the success of novel HDL-based therapies.