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Brain-infiltrating CD8+ T cell activity after acute infection and during CNS autoimmunity

ABSTRACT: Brain-infiltrating CD8+ T cell activity after acute infection and during CNS autoimmunity

PROVIDER: PRJNA629521 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11652677.fastq.gz	Fastqsanger.gz
	SRR11652678.fastq.gz	Fastqsanger.gz
	SRR11638279.fastq.gz	Fastqsanger.gz
	SRR11652679.fastq.gz	Fastqsanger.gz
	SRR11638280.fastq.gz	Fastqsanger.gz

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Brain-infiltrating CD8+ T cell transcriptional activity after acute infection and during CNS autoimmunity [RNA-Seq]

Project description:Gene expression of WT and Tox -/- P14 CD8+ T cells adoptively transfered in WT and MOG-GP recipient mice following intracranial infection with LCMV-GP. CD8+ T cells play a pivotal role in eliminating pathogens or tumors, but they equally exert tissue damage in autoimmune or chronic inflammatory diseases. While the mechanisms regulating the differentiation of CD8+ T cells in chronic infections and cancer are just beginning to be unraveled, we still lack knowledge about how this unfolds in autoimmune diseases. Here, we investigated in a model of chronic central nervous system autoimmunity, the transcriptional and epigenetic landscape of autoreactive brain infiltrating CD8+ T cells and how these cells diverge from classical long-lived memory CD8+ T emerging after virus infection.

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Brain-infiltrating CD8+ T cell transcriptional activity after acute infection and during CNS autoimmunity [RNA-Seq]

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Brain-infiltrating CD8+ T cell chromatin accessibility after acute infection and during CNS autoimmunity [ATAC-Seq]

Project description:CD8+ T cells play a pivotal role in eliminating pathogens or tumors, but they equally exert tissue damage in autoimmune or chronic inflammatory diseases. While the mechanisms regulating the differentiation of CD8+ T cells in chronic infections and cancer are just beginning to be unraveled, we still lack knowledge about how this unfolds in autoimmune diseases. Here, we investigated in a model of chronic central nervous system autoimmunity, the transcriptional and epigenetic landscape of autoreactive brain infiltrating CD8+ T cells and how these cells diverge from classical long-lived memory CD8+ T emerging after virus infection.

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Brain-infiltrating CD8+ T cell chromatin accessibility after acute infection and during CNS autoimmunity [ATAC-Seq]

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Genome-wide transcriptional analysis of CD8+ brain TRM during CNS autoimmunity

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Brain-infiltrating CD8+ T cell activity after acute infection and during CNS autoimmunity

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

2020-12-16 | GSE149643 | GEO

Genome-wide transcriptional analysis of CD8+ brain TRM during CNS autoimmunity

Project description:CD8+ TRM are described in autoimmune and chronic inflammatory diseases. However, we still lack knowledge about mechanisms regulating TRM reactivation, in particular in autoimmune diseases. Here, we investigated in a model of TRM-driven central nervous system autoimmunity the transcriptional landscape of self-reactive brain TRM and the requirement of these cells for CD4+ T cell help.

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Project description:Objective: Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system (CNS), characterized by a global increasing incidence driven by relapsing-remitting disease in females. p38 MAP kinase (MAPK) has been described as a key regulator of inflammatory responses in autoimmunity, but its role in the sexual dimorphism in MS or MS models remains unexplored. Methods: Toward this end, we used experimental autoimmune encephalomyelitis (EAE), the principal animal model of MS, combined with pharmacologic and genetic inhibition of p38 MAPK activity and transcriptomic analyses. Results: Pharmacologic inhibition of p38 MAPK selectively ameliorated EAE in female mice. Conditional deletion studies demonstrated that p38M-NM-1 signaling in macrophages/myeloid cells, but not T cells or dendritic cells, recapitulated this sexual dimorphism. Analysis of CNS inflammatory infiltrates showed that female, but not male mice lacking p38M-NM-1 in myeloid cells exhibited reduced immune cell activation compared with controls, while peripheral T cell priming was unaffected in both sexes. Transcriptomic analyses of myeloid cells revealed differences in p38M-NM-1-controlled transcripts comprising female- and male-specific gene modules, with greater p38M-NM-1 dependence of pro-inflammatory gene expression in females. Interpretation: Our findings demonstrate a key role for p38M-NM-1 in myeloid cells in CNS autoimmunity and uncover important molecular mechanisms underlying sex differences in disease pathogenesis. Taken together, our results suggest that the p38 MAPK signaling pathway represents a novel target for much needed disease modifying therapies for MS WT vs. p38alphaCKO macrophages, male vs. female

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