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Transcriptional Control of Inflammatory Responses

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Date 2014 Sep 13
PMID 25213094
Citations 66
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Abstract

The inflammatory response requires the activation of a complex transcriptional program that is both cell-type- and stimulus-specific and involves the dynamic regulation of hundreds of genes. In the context of an inflamed tissue, extensive changes in gene expression occur in both parenchymal cells and infiltrating cells of the immune system. Recently, basic transcriptional mechanisms that control inflammation have been clarified at a genome scale, particularly in macrophages and conventional dendritic cells. The regulatory logic of distinct groups of inflammatory genes can be explained to some extent by identifiable sequence-encoded features of their chromatin organization, which impact on transcription factor (TF) accessibility and impose different requirements for gene activation. Moreover, it has become apparent that the interplay between TFs activated by inflammatory stimuli and master regulators exerts a crucial role in controlling cell-type-specific transcriptional outputs.

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References
1.
Creyghton M, Cheng A, Welstead G, Kooistra T, Carey B, Steine E . Histone H3K27ac separates active from poised enhancers and predicts developmental state. Proc Natl Acad Sci U S A. 2010; 107(50):21931-6. PMC: 3003124. DOI: 10.1073/pnas.1016071107. View

2.
Struhl K, Segal E . Determinants of nucleosome positioning. Nat Struct Mol Biol. 2013; 20(3):267-73. PMC: 3740156. DOI: 10.1038/nsmb.2506. View

3.
Thomas K, Galligan C, Newman R, Fish E, Vogel S . Contribution of interferon-beta to the murine macrophage response to the toll-like receptor 4 agonist, lipopolysaccharide. J Biol Chem. 2006; 281(41):31119-30. DOI: 10.1074/jbc.M604958200. View

4.
Lichtinger M, Ingram R, Hannah R, Muller D, Clarke D, Assi S . RUNX1 reshapes the epigenetic landscape at the onset of haematopoiesis. EMBO J. 2012; 31(22):4318-33. PMC: 3501222. DOI: 10.1038/emboj.2012.275. View

5.
Natoli G, Andrau J . Noncoding transcription at enhancers: general principles and functional models. Annu Rev Genet. 2012; 46:1-19. DOI: 10.1146/annurev-genet-110711-155459. View