Genome-wide maps of EGR2 transcription factor binding sites in T cell anergy
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE46241 | GEO | 2013/04/21
SECONDARY ACCESSION(S): PRJNA198451
REPOSITORIES: GEO
Similar Datasets
Project description:We report the application of sequencing technology for mapping the EGR2 transcriptional program in T cell anergy Examination of Egr2 genomic binding sites in T cells following overnight treatment with immobilized anti-CD3 mAb (1ug/ml)
2013-04-21 | E-GEOD-46241 | biostudies-arrayexpress
Project description:We report the application of single-molecule-based sequencing technology for mapping the Egr2 transcriptional program in developing thymic NKT. We found that Egr2 controls the induction of genes required for NKT development.
2012-02-06 | GSE34254 | GEO
Project description:We report the application of single-molecule-based sequencing technology for mapping the Egr2 transcriptional program in developing thymic NKT. We found that Egr2 controls the induction of genes required for NKT development. Examination of developing NKT cells and thymocytes receiving a strong TCR signal in vivo by injecting 500ug anti-TCRb antibody.
2012-02-06 | E-GEOD-34254 | biostudies-arrayexpress
Project description:T cell anergy is one of the mechanisms contributing to peripheral tolerance, particularly in the context of progressively growing tumors and in tolerogenic treatments promoting allograft acceptance. We recently reported that early growth response gene 2 (Egr2) is a critical transcription factor for the induction of anergy in vitro and in vivo, which was identified based on its ability to regulate the expression of inhibitory signaling molecules diacylglycerol kinase (DGK)-a and -z. We reasoned that other transcriptional targets of Egr2 might encode additional factors important for T cell anergy and immune regulation. Thus, we conducted two sets of genome-wide screens: gene expression profiling of wild type versus Egr2-deleted T cells treated under anergizing conditions, and a ChIP-Seq analysis to identify genes that bind Egr2 in anergic cells. Merging of these data sets revealed 49 targets that are directly regulated by Egr2. Among these are inhibitory signaling molecules previously reported to contribute to T cell anergy, but unexpectedly, also cell surface molecules and secreted factors, including lymphocyte-activation gene 3 (Lag3), Class-I-MHC-restricted T cell associated molecule (Crtam), Semaphorin 7A (Sema7A), and chemokine CCL1. These observations suggest that anergic T cells might not simply be functionally inert, and may have additional functional properties oriented towards other cellular components of the immune system. T cell-specific Egr2 deletion was mediated by use of a Cre-expressing adenovirus and a CAR Tg x Egr2flox/flox mouse in which CAR is expressed exclusively in the T cell compartment from a Lck promoter/CD2 enhancer cassette. OVA-specific Th1 cell clones were generated from CAR Tg x Egr2flox/flox mice. CAR Tg x Egr2flox/flox Th1 T cells were infected with an empty (EV) or a Cre-expressing adenovirus. Upon confirmation of Egr2 deletion by immunoblot, the T cells were left untreated (Control) or anergized (Anergic) by immobilized anti-CD3 for 16 hours, and microarray was conducted after 1 day of rest in culture medium. The microarray analysis was performed three times using three sets of independently manipulated samples
2013-04-21 | E-GEOD-46242 | biostudies-arrayexpress
Project description:T cell anergy is one of the mechanisms contributing to peripheral tolerance, particularly in the context of progressively growing tumors and in tolerogenic treatments promoting allograft acceptance. We recently reported that early growth response gene 2 (Egr2) is a critical transcription factor for the induction of anergy in vitro and in vivo, which was identified based on its ability to regulate the expression of inhibitory signaling molecules diacylglycerol kinase (DGK)-a and -z. We reasoned that other transcriptional targets of Egr2 might encode additional factors important for T cell anergy and immune regulation. Thus, we conducted two sets of genome-wide screens: gene expression profiling of wild type versus Egr2-deleted T cells treated under anergizing conditions, and a ChIP-Seq analysis to identify genes that bind Egr2 in anergic cells. Merging of these data sets revealed 49 targets that are directly regulated by Egr2. Among these are inhibitory signaling molecules previously reported to contribute to T cell anergy, but unexpectedly, also cell surface molecules and secreted factors, including lymphocyte-activation gene 3 (Lag3), Class-I-MHC-restricted T cell associated molecule (Crtam), Semaphorin 7A (Sema7A), and chemokine CCL1. These observations suggest that anergic T cells might not simply be functionally inert, and may have additional functional properties oriented towards other cellular components of the immune system.
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Project description:T cell receptor(TCR) engagement in the absence of costimulation leads to a state of T cell tolerance known as anergy. Anergy induction requires new protein synthesis since it is inhibited by cycloheximide. In this experiment, we tried to figure out kinetic properties of the gene expression in anergy induction phase and the subsequent anergy maintenance phase.
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Project description:pooled mRNA (2, 4, 6 hrs) from A.E7 T cells under conditions which promote or inhibit anergy induction Keywords: ordered
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Project description:We provide ChIP-Seq analysis of Egr2 and Sox10 transcription factor binding in Schwann cells of rat peripheral nerve ChIP-Seq analysis of Egr2 and Sox10 binding in P15 rat sciatic nerve. Wiggle files of negative log of posterior probability determined by Mosaics.
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Project description:T cell receptor(TCR) engagement in the absence of costimulation leads to a state of T cell tolerance known as anergy. Anergy induction requires new protein synthesis since it is inhibited by cycloheximide. In this experiment, we tried to figure out kinetic properties of the gene expression in anergy induction phase and the subsequent anergy maintenance phase. A.E7 cell, a murine CD4(+) T cell clone, was stimulated with anti-TCR antibody for 0, 2, 4, and 6hrs followed by RNA extraction. For the maintenance phase, A.E7 was stimulated for 16hrs and rested for 5days before RNA extraction.
2015-11-01 | E-GEOD-72731 | biostudies-arrayexpress