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AhR signaling reprograms newly activated CD4+ T cells promoting combinatorial expression of regulatory genes to suppress murine GVHD

ABSTRACT: AhR signaling reprograms newly activated CD4+ T cells promoting combinatorial expression of regulatory genes to suppress murine GVHD

PROVIDER: PRJNA325446 | ENA |

REPOSITORIES: ENA

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AhR signaling reprograms newly activated CD4+ T cells promoting combinatorial expression of regulatory genes to suppress murine GVHD [72 hr]

Project description:AhR activation during the first 3 days of an immune response is sufficient to reprogram CD4+ T cells, resulting in prevention of GVHD. To identify the early transciptional signature of AhR activation in CD4+ T cells, we performed analyses on mice treated with 2 different AhR ligands, TCDD and Cl-BBQ, in comparison with vehicle treated mice. Transcriptional responses were measured by global microarray analysis of donor alloresponding CD4+ T cells from spleen and lymph nodes.

2016-09-01 | GSE83258 | GEO

AhR signaling reprograms newly activated CD4+ T cells promoting combinatorial expression of regulatory genes to suppress murine GVHD [48 hr]

2016-09-01 | GSE83257 | GEO

AhR signaling reprograms newly activated CD4+ T cells promoting combinatorial expression of regulatory genes to suppress murine GVHD

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

2016-09-01 | GSE83260 | GEO

AhR antagonist

Project description:AhR antagonist

| PRJNA766233 | ENA

Addition of IL-6 inhibition to standard GVHD prophylaxis to prevent GVHD after allogeneic stem cell transplantation

Project description:BACKGROUND - IL-6 mediates graft-versus-host disease (GVHD) in experimental allogeneic stem cell transplantation (alloSCT) and is an attractive therapeutic target. METHODS - A registered phase I/II study (ACTRN12612000726853) of IL-6 receptor (IL-6R) neutralizing antibody administration on day -1 to patients receiving full or reduced-intensity conditioning (RIC) and alloSCT from HLA-matched sibling or unrelated donors with standard cyclosporin and methotrexate GVHD prophylaxis. The primary endpoint was incidence of grade II-IV acute GVHD. Outcomes were compared to a non-randomized but contemporaneous group of study patients receiving the same alloSCT in the absence of IL-6R mAb. FINDINGS - Cytokine and pharmacokinetic analysis confirmed transient IL-6 dysregulation in the first month after alloSCT with complete inhibition following IL-6R mAb administration. With median follow up of 497 days, the incidence of grade II-IV GVHD was 12.5% in recipients of IL-6R inhibition (n = 48) versus 41.5% in the (n = 53) control cohort (P = 0.001). Low rates of acute GVHD were noted in patients receiving IL-6R inhibition relative to control patients following both myeloablative (12.5% vs. 46.4%, P = 0.03) and RIC (12.5% vs. 36.0%, P = 0.04). The incidence of severe (grade III/IV) acute GVHD was 4.2% in recipients of IL-6R inhibition versus 20.8% in the control cohort (P = 0.012). Relapse and chronic GVHD were unchanged. Immune reconstitution was preserved in recipients of IL-6R inhibition, but qualitatively modified with suppression of known pathogenic STAT3-dependent pathways. INTERPRETATION - IL-6 is the principal detectable and dysregulated cytokine secreted after alloSCT and its inhibition is a potential new and simple strategy to protect from acute GVHD despite robust immune reconstitution and a sustained graft-versus-leukemia effect. Single colour, Illumina Human HT12v4 Beadarrays.

2014-09-09 | E-GEOD-61201 | biostudies-arrayexpress

AhR interactome in early embryonic development

Project description:The transcriptional program of early embryonic development is tightly regulated by a set of well-defined transcription factors that suppress premature expression of differentiation genes and sustain the pluripotent identity. It is generally accepted that this program can be perturbed by environmental factors such as chemical pollutants, however the precise molecular mechanisms remain unknown. The Aryl Hydrocarbon Receptor (AHR) is a widely expressed nuclear receptor that senses environmental stimuli and modulates target gene expression. Here, we show that ectopic activation of AHR during early differentiation disrupts the differentiation program via the chromatin remodeling complex NuRD. The activated AHR/NuRD complex altered the expression of differentiation-specific genes that control the first two developmental decisions without affecting the pluripotency program. These findings identify a novel mechanism that allows environmental stimuli to disrupt embryonic development through AHR signaling.

2018-02-26 | PXD006089 | Pride

Comparison of gene expression in AhR WT (+/+) and AhR KO (-/-) primary mouse keratinocytes

Project description:The AhR is a ligand activated transcription factor that may be important in normal skin physiology. We compared gene expression profiles between AhR Wt and AhR KO primary mouse keratinocyte cultures. We identified 391 genes that were differentially expressed with a 1.5 fold cutoff and p<.05, and identified the AhR as an important regulator of genes involved in normal epidermal differentiation. AhR Wt primary keratinocyte cultures (n=4) were compared with AhR KO primary keratinocyte cultures (n=3)

2015-07-01 | E-GEOD-62490 | biostudies-arrayexpress

Mus musculus

Project description:AhR signaling reprograms newly activated CD4+ T cells promoting combinatorial expression of regulatory genes to suppress murine GVHD [72 hr]

| PRJNA325450 | ENA

Mus musculus

Project description:AhR signaling reprograms newly activated CD4+ T cells promoting combinatorial expression of regulatory genes to suppress murine GVHD [48 hr]

| PRJNA325451 | ENA

Hexokinase 2 is a transcriptional targetHexokinase 2 is a transcriptional target and a positive modulator of AHR signalling and a positive modulator of AHR signalling

Project description:The Aryl Hydrocarbon Receptor (AHR) regulates the expression of numerous genes in response to activation by agonists including xenobiotics. Although it is well appreciated that environmental signals and cell intrinsic features may modulate this transcriptional response, how it is mechanistically achieved remains poorly understood. We show that Hexokinase 2 (HK2) a metabolic enzyme fuelling cancer cell growth, is a transcriptional target of AHR as well as a modulator of its activity. Expression of HK2 is positively regulated by AHR upon exposure to agonists both in human cells and in mice lung tissues. Conversely, over-expression of HK2 regulates the abundance of many proteins involved in the regulation of AHR signalling and these changes are linked with altered AHR expression levels and transcriptional activity. HK2 expression also shows a negative correlation with AHR promoter methylation in tumours, and these tumours with high HK2 expression and low AHR methylation are associated with a worse overall survival in patients. In sum, our study provides novel insights into how AHR signalling is regulated which may help our understanding of the context-specific effects of this pathway and may have implications in cancer.

2022-05-31 | PXD028992 | Pride

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