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IFN훾-induced treatment of a Human Lung Adenocarcinoma Cell Line is Mediated by an Environmental Chemical Receptor (AhR) through PD-L1 and IDO Control (a549 bulk RNA)

ABSTRACT: IFN훾-induced treatment of a Human Lung Adenocarcinoma Cell Line is Mediated by an Environmental Chemical Receptor (AhR) through PD-L1 and IDO Control (a549 bulk RNA)

PROVIDER: PRJNA1010843 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25819747_1.fastq.gz	Fastqsanger.gz
	SRR25819747_2.fastq.gz	Fastqsanger.gz
	SRR25819748_1.fastq.gz	Fastqsanger.gz
	SRR25819748_2.fastq.gz	Fastqsanger.gz
	SRR25819749_1.fastq.gz	Fastqsanger.gz

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IFN -induced treatment of a Human Lung Adenocarcinoma Cell Line is Mediated by an Environmental Chemical Receptor (AhR) through PD-L1 and IDO Control (a549 bulk RNA)

Project description:While immunotherapy has shown efficacy in non-small cell lung cancer (NSCLC) patients, many respond only partially or not at all. One limitation in improving outcomes is the lack of a complete understanding of factors regulating immune checkpoint targets. Here, we sought to address a possible link between an environmental chemical receptor implicated in NSCLC and immune regulation, the aryl hydrocarbon receptor (AhR), and a known but counterintuitive mediator of immunosuppression, IFN , in regulation of two immune checkpoints, PD-L1 and the IDO1, in lung adenocarcinoma (LUAD). To this end we used AhR, PD-L1, and IFN R gene-edited LUAD cell lines, a syngeneic LUAD mouse model, bulk- and single cell-RNA sequencing of LUADs and tumor-infiltrating leukocytes, and existing human transcriptomic databases. The data demonstrate that: 1) the AhR regulates both PD-L1 and IDO1 in murine and human LUAD cells, 2) AhR-driven IDO1 results in production of Kyn which likely mediates an AhR→IDO1→Kyn→AhR amplification loop, 3) the previously characterized induction by IFN of PD-L1 and IDO is mediated by the AhR, 4) transplantation of LUAD cells in which the AhR is deleted results in long-term tumor immunity in approximately half of the mice; slow growing tumors in the other half exhibit significantly higher densities of CD4+ and CD8+ T cells expressing immunocompetence markers, and 5) deletion of either IFN R1 or PD-L1 does not provide the same level of immune protection as AhR deletion. The data definitively link IFN - mediated immunosuppression to the AhR and support the targeting of the AhR in the context of LUAD.

2024-06-08 | GSE241977 | GEO

IFN -induced Immunosuppression in Lung Carcinoma is Mediated by an Environmental Chemical Receptor (AhR) through PD-L1 and IDO Control (cmt167 scRNA)

2024-06-08 | GSE241979 | GEO

IFN -induced Immunosuppression in Lung Carcinoma is Mediated by an Environmental Chemical Receptor (AhR) through PD-L1 and IDO Control (cm167 bulk RNA)

2024-06-08 | GSE241978 | GEO

IFN훾-induced Immunosuppression in Lung Carcinoma is Mediated by an Environmental Chemical Receptor (AhR) through PD-L1 and IDO Control

Project description:IFN훾-induced Immunosuppression in Lung Carcinoma is Mediated by an Environmental Chemical Receptor (AhR) through PD-L1 and IDO Control

| PRJNA1010841 | ENA

IFN훾-induced Immunosuppression in Lung Carcinoma is Mediated by an Environmental Chemical Receptor (AhR) through PD-L1 and IDO Control (cmt167 scRNA)

Project description:IFN훾-induced Immunosuppression in Lung Carcinoma is Mediated by an Environmental Chemical Receptor (AhR) through PD-L1 and IDO Control (cmt167 scRNA)

| PRJNA1010847 | ENA

IFN훾-induced Immunosuppression in Lung Carcinoma is Mediated by an Environmental Chemical Receptor (AhR) through PD-L1 and IDO Control (cm167 bulk RNA)

Project description:IFN훾-induced Immunosuppression in Lung Carcinoma is Mediated by an Environmental Chemical Receptor (AhR) through PD-L1 and IDO Control (cm167 bulk RNA)

| PRJNA1010848 | ENA

AhR mutant vs N2 wild-type C.elegans, in L1 larval stage

Project description:Expression profiles of AhR mutant vs N2 wild-type C.elegans, in L1 larval stage compared by using 23232 feature WUSTL microarray 4 ahr-mutant worm samples compared to 3 wild-type samples. Total RNAs purified and reverse transcribed to cDNA and labeled with Cy3-dUTP, and then hybridized on microarray.

2010-05-16 | E-GEOD-16036 | biostudies-arrayexpress

AhR mutant vs N2 wild-type C.elegans, in L1 larval stage

Project description:Expression profiles of AhR mutant vs N2 wild-type C.elegans, in L1 larval stage compared by using 23232 feature WUSTL microarray

2009-12-19 | GSE16036 | GEO

Gene expression profiling of IDO-competent dendritic cells

Project description:Although much is known on the transcriptional profiles of dendritic cells (DCs) during maturation, the molecular switches critical for the acquisition of a tolerogenic program by DCs are still obscure. In the present study, we explored the gene expression pattern of CD8+ DCs purified from the mouse spleen and treated with interferon (IFN)-gamma. The cytokine, indeed, potentiates the tolerogenic potential of this DC subset via induction of the immunosuppressive tryptophan catabolism mediated by indoleamine 2,3-dioxygenase (IDO). By comparing the expression of the IFN-gamma-modulated genes in IDO+ versus IDO- murine DCs, we found a consistent and selective association of the IDO-competent phenotype with the down-modulation of the Tyrobp gene, encoding the adapter molecule DAP12. IFN-gamma-mediated down-modulation of this gene involved IFN consensus sequence binding protein (ICSBP), a transcription factor also known as IRF-8. While silencing of Tyrobp conferred IDO functional competence on IDO- DCs, silencing of Icsbp1 in IDO+ cells completely abolished IDO expression and function. In parallel, silencing of TYROBP conferred IDO competence on human IDO- DCs while silencing of IRF8 impaired IDO expression and activity in human IDO+ DCs. Therefore, the same small set of molecular switches controls IDO competence in murine and human DCs. Keywords: Time-course, treatment with agent (IFN-gamma)

2005-12-09 | GSE3337 | GEO

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

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