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PD-L1 positive astrocytes attenuate inflammatory functions of PD 1 positive microglia in models of autoimmune neuroinflammation [RNA-seq: IFNb]

ABSTRACT: PD-L1 positive astrocytes attenuate inflammatory functions of PD 1 positive microglia in models of autoimmune neuroinflammation [RNA-seq: IFNb]

PROVIDER: PRJNA1001314 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25491758_1.fastq.gz	Fastqsanger.gz
	SRR25491758_2.fastq.gz	Fastqsanger.gz
	SRR25491759_1.fastq.gz	Fastqsanger.gz
	SRR25491759_2.fastq.gz	Fastqsanger.gz
	SRR25491760_1.fastq.gz	Fastqsanger.gz

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PD-L1 positive astrocytes attenuate inflammatory functions of PD 1 positive microglia in models of autoimmune neuroinflammation

Project description:PD-L1 positive astrocytes attenuate inflammatory functions of PD 1 positive microglia in models of autoimmune neuroinflammation

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PD-L1 positive astrocytes attenuate inflammatory functions of PD 1 positive microglia in models of autoimmune neuroinflammation [RNA-seq: BMS202]

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PD-L1 positive astrocytes attenuate inflammatory functions of PD 1 positive microglia in models of autoimmune neuroinflammation [RNA-seq: IFNb]

Project description:Multiple Sclerosis (MS) is a chronic autoimmune inflammatory disorder of the central nervous system (CNS). Current therapies mainly target inflammatory processes during acute stages, but effective treatments for progressive MS are limited. In this context, astrocytes have gained increasing attention as they have the capacity to drive, but also suppress tissue-degeneration. Here we show that astrocytes upregulate the immunomodulatory checkpoint molecule PD-L1 during acute autoimmune CNS inflammation in response to aryl hydrocarbon receptor and interferon signaling. Using CRISPR-Cas9 genetic perturbation in combination with small-molecule and antibody-mediated inhibition of PD-L1 and PD-1 both in vivo and in vitro, we demonstrate that astrocytic PD-L1 and its interaction with microglial PD-1 is required for the attenuation of autoimmune CNS inflammation in acute and progressive stages in a mouse model of MS. Our findings suggest the glial PD-L1 / PD-1 axis as a new therapeutic target for both acute and progressive MS stages.

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PD-L1 positive astrocytes attenuate inflammatory functions of PD 1 positive microglia in models of autoimmune neuroinflammation [RNA-seq: BMS202]

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Expression data in PD-L1 positive and PD-L1 negative human melanoma samples

Project description:Blocking the PD-1/PD-L1 immunosuppressive pathway has shown promise in the treatment of certain cancers including melanoma. This study investigates differences in the gene expression profiles of human melanomas that do or do not display the immunosuppressive protein PD-L1. Further understanding of genes expressed within the tumor microenvironment of PD-L1+ tumors may lead to improved rationally designed treatments. Gene expression profiling was performed on total RNA extracted by laser capture microdissection from 11 archived formalin-fixed paraffin-embedded (FFPE) melanoma specimens, 5 of which were PD-L1 positive and 6 PD-L1 negative. Details of the design, and the gene signatures found are given in the paper associated with this GEO Series: Janis M. Taube, Geoffrey D. Young, Tracee L. McMiller, Shuming Chen, January T. Salas, Theresa S. Pritchard, Haiying Xu, Alan K. Meeker, Jinshui Fan, Chris Cheadle, Alan E. Berger, Drew M. Pardoll, and Suzanne L. Topalian, Differential expression of immune-regulatory genes associated with PD-L1 display in melanoma: implications for PD-1 pathway blockade, Clin Cancer Res 2015, in press.

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PD-L1 positive astrocytes attenuate inflammatory functions of PD-1 positive microglia in models of autoimmune neuroinflammation.

Project description:Multiple Sclerosis (MS) is a chronic autoimmune inflammatory disorder of the central nervous system (CNS). Current therapies mainly target inflammatory processes during acute stages, but effective treatments for progressive MS are limited. In this context, astrocytes have gained increasing attention as they have the capacity to drive, but also suppress tissue-degeneration. Here we show that astrocytes upregulate the immunomodulatory checkpoint molecule PD-L1 during acute autoimmune CNS inflammation in response to aryl hydrocarbon receptor and interferon signaling. Using CRISPR-Cas9 genetic perturbation in combination with small-molecule and antibody-mediated inhibition of PD-L1 and PD-1 both in vivo and in vitro, we demonstrate that astrocytic PD-L1 and its interaction with microglial PD-1 is required for the attenuation of autoimmune CNS inflammation in acute and progressive stages in a mouse model of MS. Our findings suggest the glial PD-L1/PD-1 axis as a potential therapeutic target for both acute and progressive MS stages.

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BTLA and PD-1 signals attenuate TCR-mediated gene expression

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PD-L1 positive astrocytes attenuate inflammatory functions of PD 1 positive microglia in models of autoimmune neuroinflammation

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

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