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Inhibition of Bromodomain and Extra Terminal (BET) domain activity modulates the IL-23R/IL17 axis and suppresses acute Graft-Versus-Host Disease [ChIP-seq]

ABSTRACT: Inhibition of Bromodomain and Extra Terminal (BET) domain activity modulates the IL-23R/IL17 axis and suppresses acute Graft-Versus-Host Disease [ChIP-seq]

PROVIDER: PRJNA762282 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15838083.fastq.gz	Fastqsanger.gz
	SRR15838084.fastq.gz	Fastqsanger.gz
	SRR15838085.fastq.gz	Fastqsanger.gz
	SRR15838086.fastq.gz	Fastqsanger.gz
	SRR15838087.fastq.gz	Fastqsanger.gz

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Inhibition of Bromodomain and Extra Terminal (BET) domain activity modulates the IL-23R/IL17 axis and suppresses acute Graft-Versus-Host Disease

Project description:Inhibition of Bromodomain and Extra Terminal (BET) domain activity modulates the IL-23R/IL17 axis and suppresses acute Graft-Versus-Host Disease

| PRJNA762276 | ENA

Inhibition of Bromodomain and Extra Terminal (BET) domain activity modulates the IL-23R/IL17 axis and suppresses acute Graft-Versus-Host Disease [RNA-Seq]

Project description:Inhibition of Bromodomain and Extra Terminal (BET) domain activity modulates the IL-23R/IL17 axis and suppresses acute Graft-Versus-Host Disease [RNA-Seq]

| PRJNA762284 | ENA

Inhibition of Bromodomain and Extra Terminal (BET) domain activity modulates the IL-23R/IL17 axis and suppresses acute Graft-Versus-Host Disease [RNA-Seq]

Project description:Acute graft-versus-host disease (GVHD) is the major cause of non-relapse mortality post-allogeneic stem cell transplantation. The majority of patients non-responsive to front line treatment with steroids have an estimated overall 2-year survival rate of only 10%. Treatment options for steroid-refractory acute GVHD are limited. Bromodomain and Extraterminal Domain (BET) inhibitors PLX51107 and PLX2853, deemed safe in human clinical trials in high risk malignancies, significantly downregulate pro-inflammatory Th1 and Th17 responses without impacting T regulatory cells, improving survival in murine models of acute GVHD while retaining beneficial graft-versus-leukemia effects. Modulation of the IL23/STAT3 axis via BET inhibition resulted in a reduction of pathogenic Th1/Th17 cells in the spleen and acute GVHD target organs such as the gastrointestinal tract. Based on our preclinical data presented here, PLX51107 will enter clinical trial for refractory acute GVHD in a Phase 1 safety, biological efficacy trial.

2021-09-12 | GSE183884 | GEO

Inhibition of Bromodomain and Extra Terminal (BET) domain activity modulates the IL-23R/IL17 axis and suppresses acute Graft-Versus-Host Disease [ChIP-seq]

2021-09-12 | GSE183883 | GEO

Inhibition of Bromodomain and Extra Terminal (BET) domain activity modulates the IL-23R/IL17 axis and suppresses acute Graft-Versus-Host Disease

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-09-12 | GSE183886 | GEO

BET bromodomain inhibition suppresses TH17-mediated pathology

Project description:IL-17-producing T helper (TH17) cells have been selected through evolution for their ability to control fungal and bacterial infections. It is also firmly established that their aberrant generation and activation results in autoimmune conditions. Using a characterized potent and selective small molecule inhibitor, we show that the bromodomain and extra-terminal domain (BET) family of chromatin adaptors plays fundamental and selective roles in human and murine TH17 differentiation from naM-CM-/ve CD4+ T cells, as well as in the activation of previously differentiated TH17 cells. We provide evidence that BET controls TH17 differentiation in a bromodomain-dependent manner through a mechanism that includes the direct regulation of multiple effector TH17-associated cytokines, including IL17, IL21 and GMCSF. We also demonstrate that BET family members Brd2 and Brd4 associate with the Il17 locus in TH17 cells, and that this association requires bromodomains. We recapitulate the critical role of BET bromodomains in TH17 differentiation in vivo and show that therapeutic dosing of the BET inhibitor is efficacious in mouse models of autoimmunity. Our results identify the BET family of proteins as a fundamental link between chromatin signaling and TH17 biology, and support the notion of BET inhibition as a point of therapeutic intervention in autoimmune conditions. 4 samples were analyzed: two conditions in duplicate. Naive T cells were placed in conditions leading to TH17 differentiation, with and without BET inhibitor. RNA was collected at 48 hours.

2013-09-20 | E-GEOD-37270 | biostudies-arrayexpress

Project description:Inhibition of Bromodomain and Extra Terminal (BET) domain activity modulates the IL-23R/IL17 axis and suppresses acute Graft-Versus-Host Disease

| PRJNA757357 | ENA

BET bromodomain inhibition suppresses TH17-mediated pathology

Project description:IL-17-producing T helper (TH17) cells have been selected through evolution for their ability to control fungal and bacterial infections. It is also firmly established that their aberrant generation and activation results in autoimmune conditions. Using a characterized potent and selective small molecule inhibitor, we show that the bromodomain and extra-terminal domain (BET) family of chromatin adaptors plays fundamental and selective roles in human and murine TH17 differentiation from naïve CD4+ T cells, as well as in the activation of previously differentiated TH17 cells. We provide evidence that BET controls TH17 differentiation in a bromodomain-dependent manner through a mechanism that includes the direct regulation of multiple effector TH17-associated cytokines, including IL17, IL21 and GMCSF. We also demonstrate that BET family members Brd2 and Brd4 associate with the Il17 locus in TH17 cells, and that this association requires bromodomains. We recapitulate the critical role of BET bromodomains in TH17 differentiation in vivo and show that therapeutic dosing of the BET inhibitor is efficacious in mouse models of autoimmunity. Our results identify the BET family of proteins as a fundamental link between chromatin signaling and TH17 biology, and support the notion of BET inhibition as a point of therapeutic intervention in autoimmune conditions.

2013-09-20 | GSE37270 | GEO

Inhibition of histone readers bromodomain extra-terminal proteins alleviates scleroderma fibrosis

Project description:Inhibition of histone readers bromodomain extra-terminal proteins alleviates scleroderma fibrosis

| PRJNA776895 | ENA

ChIPSeq data from melanoma cancer cell line CHL-1 after Bromodomain and extra terminal (Bet) domain inhibitor treatment

Project description:Bromodomain and extra terminal domain (BET) inhibition reduces occupancy of BET-family proteins at promoter and enhancer sites finally leading to genome wide changes in gene transcription. We used ChIPSeq profiling to investigate genome wide changes in promoter and enhancer occupancy induced by BET inhibitors BAY 1238097 and OTX-015, respectively.

2017-09-30 | GSE95585 | GEO

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