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

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

PROVIDER: PRJNA1001312 | ENA |

REPOSITORIES: ENA

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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: IFNb]

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

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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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Oligodendrocyte regulation during autoimmune neuroinflammation

Project description:Oligodendrocyte regulation during autoimmune neuroinflammation

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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.

| S-EPMC10492803 | biostudies-literature

Oligodendrocyte regulation during autoimmune neuroinflammation

Project description:The present study had the purpose to analyze the transcriptional state of oligodendrocytes in an animal model of multiple scleroris resembling autoimmune neuroinflammation and compared with control mice treated with ovalbumin. The results revealed that oligodendrocytes from the EAE (experimental autoimmune encephalomyelitis) model upregulate genes that are involved in immune processes providing evidence that oligodendrocytes can develop an immune phenotype in particular neuroinflammatory conditions.

2021-08-21 | GSE182341 | GEO

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.

2023-08-02 | GSE239875 | GEO

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.

2015-05-01 | E-GEOD-65041 | biostudies-arrayexpress

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Project description:Microglial activation during neuroinflammation is crucial for coordinating the immune response against neuronal tissue and the initial response of microglia determines the severity of neuroinflammatory diseases. CD83 has been associated with early activation of microglia in various disease settings albeit its functional relevance for microglial biology was still elusive. Thus, we conducted a thorough assessment of CD83 regulation in microglia as well as its impact on microglial mediated neuroinflammation. Here, we describe for the first time that CD83 expression in microglia is not only associated with cellular activation but also with pro-resolving functions. Conditional deletion of CD83 causes malfunctioning responses to myelin debris, which results in an over-activated state during autoimmune neuroinflammation. Subsequently, CD83-deficient microglia recruit more pathogenic immune cells to the central nervous system and deteriorate resolving mechanism, which exacerbates the disease. Thus, CD83 in microglia orchestrates cellular activation and consequently, also resolution of neuroinflammation.

2023-06-28 | GSE230753 | GEO

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