Histone deacetylases as regulators of inflammation and immunity

被引:463
作者
Shakespear, Melanie R. [1 ]
Halili, Maria A. [1 ]
Irvine, Katharine M. [1 ]
Fairlie, David P. [1 ]
Sweet, Matthew J. [1 ]
机构
[1] Univ Queensland, Inst Mol Biosci, Brisbane, Qld 4072, Australia
基金
澳大利亚研究理事会; 英国医学研究理事会;
关键词
NF-KAPPA-B; PROINFLAMMATORY GENE-EXPRESSION; MACROPHAGE DIFFERENTIATION; NEGATIVE REGULATION; HDAC INHIBITORS; ACETYLATION; TRANSCRIPTION; ACTIVATION; IDENTIFICATION; FAMILY;
D O I
10.1016/j.it.2011.04.001
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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.
引用
收藏
页码:335 / 343
页数:9
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