NDLI: Twist1 regulates Ifng expression in Th1 cells by interfering with Runx3 function.

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Twist1 regulates Ifng expression in Th1 cells by interfering with Runx3 function.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Vincentz, Joshua W. Kaplan, Mark H. Pham, Duy Firulli, Anthony B.
Description	Country affiliation: United States Author Affiliation: Pham D ( Department of Pediatrics, Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202, USA.)
Abstract	A transcription factor network that includes STAT4, T-bet, and Runx3 promotes the differentiation of Th1 cells and inflammatory immune responses. How additional transcription factors regulate the function of Th1 cells has not been defined. In this study we show that the negative regulatory factor Twist1 decreases expression of T-bet, Runx3, and IL-12Rß2 as it inhibits IFN-Î³ production. Ectopic expression of Runx3, but not T-bet or IL-12Rß2, compensates for the effects of Twist1 on IFN-Î³ production, and Twist1 regulation of Ifng depends on complex formation with Runx3. Twist1 decreases Runx3 and T-bet binding at the Ifng locus, and it decreases chromatin looping within the Ifng locus. These data define an IL-12/STAT4-induced negative regulatory loop that impacts multiple components of the Th1 transcriptional network and provide further insight into regulation of Th1 differentiation.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1200854
Journal	The Journal of Immunology
Issue Number	2
Volume Number	189
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2012-07-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Core Binding Factor Alpha 3 Subunit Antagonists & Inhibitors Physiology Interferon-gamma Biosynthesis Nuclear Proteins Th1 Cells Immunology Metabolism Twist Transcription Factor Animals Cells, Cultured Genetics Down-regulation Inflammation Prevention & Control Mice Mice, Inbred C57bl Mice, Knockout Mice, Transgenic Stat4 Transcription Factor Deficiency T-box Domain Proteins Research Support, N.i.h., Extramural Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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Opposing roles of STAT4 and Dnmt3a in Th1 gene regulation.

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T-bet dependent removal of Sin3A-histone deacetylase complexes at the Ifng locus drives Th1 differentiation.

STAT4 serine phosphorylation is critical for IL-12-induced IFN-gamma production but not for cell proliferation.

STAT4 isoforms differentially regulate Th1 cytokine production and the severity of inflammatory bowel disease.

Cutting edge: the pathogenicity of IFN-Î³-producing Th17 cells is independent of T-bet.

Intestinal irradiation and fibrosis in a Th1-deficient environment.

Twist1 regulates Ifng expression in T helper 1 cells by interfering with Runx3 function

Cutting edge: influence of Tmevpg1, a long intergenic noncoding RNA, on the expression of Ifng by Th1 cells.

Twist1 regulates Ifng expression in Th1 cells by interfering with Runx3 function.

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Opposing roles of STAT4 and Dnmt3a in Th1 gene regulation.

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T-bet dependent removal of Sin3A-histone deacetylase complexes at the Ifng locus drives Th1 differentiation.

STAT4 serine phosphorylation is critical for IL-12-induced IFN-gamma production but not for cell proliferation.

STAT4 isoforms differentially regulate Th1 cytokine production and the severity of inflammatory bowel disease.

Cutting edge: the pathogenicity of IFN-Î³-producing Th17 cells is independent of T-bet.

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Twist1 regulates Ifng expression in T helper 1 cells by interfering with Runx3 function

Cutting edge: influence of Tmevpg1, a long intergenic noncoding RNA, on the expression of Ifng by Th1 cells.

Twist1 regulates Ifng expression in Th1 cells by interfering with Runx3 function.