Histone deacetylases as regulators of inflammation and immunity

Shakespear, Melanie R., Halili, Maria A., Irvine, Katharine M., Fairlie, David P. and Sweet, Matthew J. (2011) Histone deacetylases as regulators of inflammation and immunity. Trends in Immunology, 32 7: 335-343. doi:10.1016/j.it.2011.04.001


Author Shakespear, Melanie R.
Halili, Maria A.
Irvine, Katharine M.
Fairlie, David P.
Sweet, Matthew J.
Title Histone deacetylases as regulators of inflammation and immunity
Journal name Trends in Immunology   Check publisher's open access policy
ISSN 1471-4906
1471-4981
0167-5699
Publication date 2011-07
Sub-type Critical review of research, literature review, critical commentary
DOI 10.1016/j.it.2011.04.001
Volume 32
Issue 7
Start page 335
End page 343
Total pages 9
Place of publication London, U.K.
Publisher Elsevier; Trends Journals
Collection year 2012
Language eng
Formatted abstract
Histone deacetylases (HDACs) remove an acetyl group from lysine residues of target proteins to regulate cellular processes. Small-molecule inhibitors of HDACs cause cellular growth arrest, differentiation and/or apoptosis, and some are used clinically as anticancer drugs. In animal models, HDAC inhibitors are therapeutic for several inflammatory diseases, but exacerbate atherosclerosis and compromise host defence. Loss of HDAC function has also been linked to chronic lung diseases in humans. These contrasting effects might reflect distinct roles for individual HDACs in immune responses. Here, we review the current understanding of innate and adaptive immune pathways that are regulated by classical HDAC enzymes. The objective is to provide a rationale for targeting (or not targeting) individual HDAC enzymes with inhibitors for future immune-related applications.
Keyword NF-kappa-B
Hypoxia-inducible factor-1-alpha
Proinflammatory gene-expression
Macrophage differentiation
Glucocorticoid-receptor
Reversible acetylation
Negative regulation
Signaling pathway
HDAC inhibitors
Cell-function
NF-κB
Hypoxia-inducible factor-1-α
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Critical review of research, literature review, critical commentary
Collections: Official 2012 Collection
Institute for Molecular Bioscience - Publications
 
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