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CXCR6 orchestrates brain CD8+ T cell residency and limits mouse Alzheimer’s disease pathology [scRNA-seq4]

ABSTRACT: Our study reveals a previously unappreciated role for microenvironment-specific, inter-cellular crosstalk between CD8+ T cells and microglia in delaying neurodegenerative disease development

ORGANISM(S): Mus musculus

PROVIDER: GSE233463 | GEO | 2023/08/17

REPOSITORIES: GEO

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CXCR6 orchestrates brain CD8<sup>+</sup> T cell residency and limits mouse Alzheimer's disease pathology.

Project description:Neurodegenerative diseases, including Alzheimer's disease (AD), are characterized by innate immune-mediated inflammation, but functional and mechanistic effects of the adaptive immune system remain unclear. Here we identify brain-resident CD8+ T cells that coexpress CXCR6 and PD-1 and are in proximity to plaque-associated microglia in human and mouse AD brains. We also establish that CD8+ T cells restrict AD pathologies, including β-amyloid deposition and cognitive decline. Ligand-receptor interaction analysis identifies CXCL16-CXCR6 intercellular communication between microglia and CD8+ T cells. Further, Cxcr6 deficiency impairs accumulation, tissue residency programming and clonal expansion of brain PD-1+CD8+ T cells. Ablation of Cxcr6 or CD8+ T cells ultimately increases proinflammatory cytokine production from microglia, with CXCR6 orchestrating brain CD8+ T cell-microglia colocalization. Collectively, our study reveals protective roles for brain CD8+ T cells and CXCR6 in mouse AD pathogenesis and highlights that microenvironment-specific, intercellular communication orchestrates tissue homeostasis and protection from neuroinflammation.

| S-EPMC11102766 | biostudies-literature