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Transcription profiling of mouse wild type or Batf deficient T cells cultured under various combinations of IL-6 orTGF-beta

ABSTRACT: Wild type and Batf deficient T cells were stimulated under various combinations of IL-6 or TGF-beta.

ORGANISM(S): Mus musculus

SUBMITTER: Barbara Schraml

PROVIDER: E-MEXP-2152 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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The AP-1 transcription factor Batf controls T(H)17 differentiation.

Schraml Barbara U BU Hildner Kai K Ise Wataru W Lee Wan-Ling WL Smith Whitney A-E WA Solomon Ben B Sahota Gurmukh G Sim Julia J Mukasa Ryuta R Cemerski Saso S Hatton Robin D RD Stormo Gary D GD Weaver Casey T CT Russell John H JH Murphy Theresa L TL Murphy Kenneth M KM

Nature 20090705 7253

Activator protein 1 (AP-1, also known as JUN) transcription factors are dimers of JUN, FOS, MAF and activating transcription factor (ATF) family proteins characterized by basic region and leucine zipper domains. Many AP-1 proteins contain defined transcriptional activation domains, but BATF and the closely related BATF3 (refs 2, 3) contain only a basic region and leucine zipper, and are considered to be inhibitors of AP-1 activity. Here we show that Batf is required for the differentiation of IL ...[more]

PMID: 19578362

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2010-08-31 | E-GEOD-23505 | biostudies-arrayexpress

Dynamic BRG1 Recruitment During T Helper Differentiation And Activation Reveals Distal Regulatory Elements

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Project description:Through their functional diversification, CD4+ T cells play key roles in both driving and constraining immune-mediated pathology. Transcription factors are critical in the generation and maintenance of cellular diversity and negative regulators antagonistic to alternate fates often act in conjunction with positive regulators to stabilize lineage specification1. Polymorphisms within the locus encoding a transcription factor BACH2 are associated with diverse immune-mediated diseases including asthma2, multiple sclerosis3, Crohn¹s disease4-5, coeliac disease6, vitiligo7 and type 1 diabetes8. A role for Bach2 in maintaining immune homeostasis, however, has not been established. Here, we define Bach2 as a broad regulator of immune activation that stabilizes immunoregulatory capacity while repressing the differentiation programmes of multiple effector lineages in CD4+ T cells. Bach2 was required for efficient formation of regulatory (Treg) cells and consequently for suppression of lethal inflammation in a manner that was Treg cell dependent. Assessment of the genome-wide function of Bach2, however, revealed that it represses genes associated with effector cell differentiation. Consequently, its absence during Treg polarization resulted in inappropriate diversion to effector lineages. In addition, Bach2 constrained full effector differentiation within Th1, Th2 and Th17 cell lineages. These findings identify Bach2 as a key regulator of CD4+ T-cell differentiation that prevents inflammatory disease by controlling the balance between tolerance and immunity. The role of Bach2t to regulate immune homeostasis was investigated by mapping DNA binding profiles of Bach2 in iTreg condition. The function of Bach2 was also evaluated by comparing transcriptome in WT and Bach2-deficient iTreg cells and further comparison was done with transcriptome in naive, Th1, Th2, and Th17 conditions.

2013-06-27 | E-GEOD-45975 | biostudies-arrayexpress

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2014-03-26 | E-GEOD-44937 | biostudies-arrayexpress

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2014-02-13 | E-GEOD-54938 | biostudies-arrayexpress

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