Datasets

Title	IFN-g Regulates mTORC1, Cellular Metabolism and mRNA Translation to Potentiate Inflammatory Macrophage Activation [miRNA-Seq]
Organism	Homo sapiens
Number of Samples	8
Release Date	2015/03/12 00:00
Sequencing Types
Protocol Details

Title
Authors	Su X,Yu Y,Zhong Y,Giannopoulou EG,Hu X,Liu H,Cross JR,Rätsch G,Rice CM,Ivashkiv LB
Journal	Nature immunology
Publication Date	2015 Aug
Abstract	Interferon-γ (IFN-γ) primes macrophages for enhanced microbial killing and inflammatory activation by Toll-like receptors (TLRs), but little is known about the regulation of cell metabolism or mRNA translation during this priming. We found that IFN-γ regulated the metabolism and mRNA translation of human macrophages by targeting the kinases mTORC1 and MNK, both of which converge on the selective regulator of translation initiation eIF4E. Physiological downregulation of mTORC1 by IFN-γ was associated with autophagy and translational suppression of repressors of inflammation such as HES1. Genome-wide ribosome profiling in TLR2-stimulated macrophages showed that IFN-γ selectively modulated the macrophage translatome to promote inflammation, further reprogram metabolic pathways and modulate protein synthesis. These results show that IFN-γ-mediated metabolic reprogramming and translational regulation are key components of classical inflammatory macrophage activation.
PMC	PMC4509841
PMID	26147685
DOI

Su et al. 2015 (PRJNA278007)