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miR-155 activates cytokine gene expression in Th17 cells by regulating the DNA-binding protein Jarid2 to relieve polycomb-mediated repression.

Abstract：

:Specification of the T helper 17 (Th17) cell lineage requires a well-defined set of transcription factors, but how these integrate with posttranscriptional and epigenetic programs to regulate gene expression is poorly understood. Here we found defective Th17 cell cytokine expression in miR-155-deficient CD4+ T cells in vitro and in vivo. Mir155 was bound by Th17 cell transcription factors and was highly expressed during Th17 cell differentiation. miR-155-deficient Th17 and T regulatory (Treg) cells expressed increased amounts of Jarid2, a DNA-binding protein that recruits the Polycomb Repressive Complex 2 (PRC2) to chromatin. PRC2 binding to chromatin and H3K27 histone methylation was increased in miR-155-deficient cells, coinciding with failure to express Il22, Il10, Il9, and Atf3. Defects in Th17 cell cytokine expression and Treg cell homeostasis in the absence of Mir155 could be partially suppressed by Jarid2 deletion. Thus, miR-155 contributes to Th17 cell function by suppressing the inhibitory effects of Jarid2.

journal_name

Immunity

journal_title

Immunity

authors

Escobar TM,Kanellopoulou C,Kugler DG,Kilaru G,Nguyen CK,Nagarajan V,Bhairavabhotla RK,Northrup D,Zahr R,Burr P,Liu X,Zhao K,Sher A,Jankovic D,Zhu J,Muljo SA

doi

10.1016/j.immuni.2014.03.014

subject

Has Abstract

pub_date

2014-06-19 00:00:00

pages

865-79

issue

6

eissn

1074-7613

issn

1097-4180

pii

S1074-7613(14)00157-5

journal_volume

40

pub_type

杂志文章

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