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Eph Receptor B3/EphrinB3 signaling impact CNS pathology during EAE

ABSTRACT: Eph Receptor B3/EphrinB3 signaling impact CNS pathology during EAE

PROVIDER: PRJNA627212 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11583500_1.fastq.gz	Fastqsanger.gz
	SRR11583500_2.fastq.gz	Fastqsanger.gz
	SRR11583501_1.fastq.gz	Fastqsanger.gz
	SRR11583501_2.fastq.gz	Fastqsanger.gz
	SRR11583502_1.fastq.gz	Fastqsanger.gz

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Eph Receptor B3/EphrinB3 signaling impact CNS pathology during EAE

Project description:We aimed to investigate the role of EphB3 and EfnB3 on the regulation of astrocyte and microglial responses in the context of CNS inflammation, we KD Efnb3 in microglia or EphB3 in astrocytes both resulting in a comparable amelioration of EAE. The transcriptional analysis of the two cell types revealed the decreased expression of genes associated to inflammation and neurodegeneration in both KD conditions.

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Expression data of CNS T cells during EAE

Project description:In the absence of NR4A2 in T cells mice do not develop early acute EAE, but only a late chronic disease. We examined the mechanism by which NR4A2 can control the pathogencity of T cells in CNS autoimmune disease. To determine how NR4A2 is involved is involved in T cell pathology, we examined expression profiles of T cells during early and late diease in the presence or genetic CD4-specific absence of NR4A2. T cells infiltrating CNS tissues were isolated at peal acute EAE (D18) or during late,chronic EAE (D32). RNA expression was then analysed by genechip to determine the influence of NR4A2 in T cells on these disease stages

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Expression data of CNS T cells during EAE

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Brd4 expression in microglia supports microglial activation, T cell recruitment, and demyelination in EAE

Project description:In EAE, a mouse model of multiple sclerosis, immunization with MOG autoantigen results in the generation of Th1/Th17 T cells in the periphery. MOG antigen-specific T cells then invade into the central nervous system (CNS) resulting in neuronal demyelination. Microglia, specialized innate immune cells in the CNS, have been suggested to participate in the pathogenesis of EAE. Bromodomain inhibitors have been reported to reduce EAE pathology by inhibiting T cells. However, the contribution of BRD4 in EAE pathology is unknown. In this study, we demonstrate that microglia-specific Brd4 conditional knockout (cKO) mice, displayed markedly reduced EAE pathology. Brd4cKO microglia failed to express inflammation and activation-related genes and had reduced CNS T cell invasion. Moreover, Brd4cKO microglia: invading T cell interactions were markedly reduced, suggesting that Brd4-dependent microglial genes may play important roles in facilitating T cell restimulation within the CNS. In summary, our results demonstrate a model in which microglial BRD4 plays a key role in supporting neuroinflammation in EAE.

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Project description:Extensive cellular heterogeneity exists within specific immune-cell subtypes classified as a single lineage, but its molecular underpinnings are rarely characterized at a genomic scale. Here, we use single-cell RNA-seq to investigate the molecular mechanisms governing heterogeneity and pathogenicity of Th17 cells isolated from the central nervous system (CNS) and lymph nodes (LN) at the peak of autoimmune encephalomyelitis (EAE) or polarized in vitro under either pathogenic or non-pathogenic differentiation conditions. Computational analysis reveals a spectrum of cellular states in vivo, including a self-renewal state, Th1-like effector/memory states and a dysfunctional/senescent state. Relating these states to in vitro differentiated Th17 cells, unveils genes governing pathogenicity and disease susceptibility. Using knockout mice, we validate four novel genes: Gpr65, Plzp, Toso and Cd5l (in a companion paper). Cellular heterogeneity thus informs Th17 function in autoimmunity, and can identify targets for selective suppression of pathogenic Th17 cells while sparing non-pathogenic tissue-protective ones. Single-cell transcriptional profiling of Th17 cells, harvested at peak of disease in EAE from CNS

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Project description:We evaluated the role of EphB3 on the regulation of astrocyte and microglial responses and its potential as a therapeutic target during progressive EAE. We induced EAE in NOD mice that will develop a progressive form of the disease. Starting at the beginning of the progressive phase, A38 was administered and alternatively EphB3 was KD in astrocytes. Both treatments ameliorated the EAE. The transcriptional analysis of astrocytes and microglia revealed the decreased expression of genes associated to inflammation and neurodegeneration in both conditions.

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scRNAseq of C3 producing myeloid and astrocytic cells from EAE inflamed murine CNS [scRTL]

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