Inflammatory signalling as mediator of epigenetic modulation in tissue-specific chronic inflammation

被引：94

作者：

Baeckdahl, Liselotte ^{[1
]}

Bushell, Andrew ^{[2
]}

Beck, Stephan ^{[1
]}

机构：

[1] UCL, Inst Canc, Med Genom Grp, London WC1E 6BT, England

[2] Univ Oxford, John Radcliffe Hosp, Nuffield Dept Surg, Transplantat Res Immunol Grp, Oxford OX3 9DU, England

来源：

INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY | 2009年 / 41卷 / 01期

关键词：

Epigenetics; Chronic inflammation; Epigenetic regulation; T cells; Inflammatory diseases; NF-KAPPA-B; HISTONE DEACETYLASE INHIBITOR; ABERRANT DNA METHYLATION; LUPUS-LIKE DISEASE; T-CELL ACTIVATION; EXPERIMENTAL COLITIS; MULTIPLE-SCLEROSIS; GENE-EXPRESSION; CUTTING EDGE; TRANSCRIPTION;

D O I：

10.1016/j.biocel.2008.08.023

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Recent Successes of therapeutic intervention in chronic inflammatory diseases using epigenetic modifiers Such as historic deacetylase inhibitors and inhibitors of DNA methylation Suggest that epigenetic reprogramming plays a role in the aetiology of these diseases. The epigenetic signature of a given immune cell is reflected in the history of modifications from different signals the cell has been subjected to during differentiation. Like other cells, differentiating immune cells are dependent on a complex combination of inter- and intracell signalling as well as transcription machineries to modulate their epigenomes ill order to mediate differentiation. Despite extensive research into these processes, the link between cellular signalling and epigenetic modulation remains poorly understood. Here, we review recent progress and discuss key factors driving epigenetic modulation in chronic inflammation. (C) 2008 Elsevier Ltd. All rights reserved.

引用

页码：176 / 184

页数：9

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