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

Abstract：

:High-density lipoprotein (HDL) mediates reverse cholesterol transport and 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 regulator ATF3, as an HDL-inducible target gene in macrophages that downregulates the expression of Toll-like receptor (TLR)-induced proinflammatory 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 new HDL-based therapies.

journal_name

Nat Immunol

journal_title

Nature immunology

authors

De Nardo D,Labzin LI,Kono H,Seki R,Schmidt SV,Beyer M,Xu D,Zimmer S,Lahrmann C,Schildberg FA,Vogelhuber J,Kraut M,Ulas T,Kerksiek A,Krebs W,Bode N,Grebe A,Fitzgerald ML,Hernandez NJ,Williams BR,Knolle P,Kneillin

doi

10.1038/ni.2784

subject

Has Abstract

pub_date

2014-02-01 00:00:00

pages

152-60

issue

2

eissn

1529-2908

issn

1529-2916

pii

ni.2784

journal_volume

15

pub_type

杂志文章

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