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Regulation of CD4 T‐cell differentiation and inflammation by repressive histone methylation
Author(s) -
Antignano Frann,
Zaph Colby
Publication year - 2015
Publication title -
immunology and cell biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.999
H-Index - 104
eISSN - 1440-1711
pISSN - 0818-9641
DOI - 10.1038/icb.2014.115
Subject(s) - epigenetics , biology , cellular differentiation , histone , microbiology and biotechnology , histone h3 , prc2 , lineage (genetic) , embryonic stem cell , gene silencing , histone methyltransferase , histone methylation , dna methylation , genetics , gene , gene expression
Repressive epigenetic modifications such as dimethylation and trimethylation histone H3 at lysine 9 (H3K9me2 and H3K9me3) and H3K27me3 have been shown to be critical for embryonic stem (ES) cell differentiation by silencing cell lineage‐promiscuous genes. CD4 + T helper (T H ) cell differentiation is a powerful model to study the molecular mechanisms associated with cellular lineage choice in adult cells. Naïve T H cells have the capacity to differentiate into one of the several phenotypically and functionally distinct and stable lineages. Although some repressive epigenetic mechanisms have a critical role in T H cell differentiation in a similar manner to that in ES cells, it is clear that there are disparate functions for certain modifications between ES cells and T H cells. Here we review the role of repressive histone modifications in the differentiation and function of T H cells in health and disease.