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RNA-seq of Zbtb10 Knockdown and Control cDC1 dendritic cells (Cd8+)

ABSTRACT: RNA-seq of Zbtb10 Knockdown and Control cDC1 dendritic cells (Cd8+)

PROVIDER: PRJEB40082 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR4552430_1.fastq.gz	Fastqsanger.gz
	ERR4552430_2.fastq.gz	Fastqsanger.gz
	ERR4552431_1.fastq.gz	Fastqsanger.gz
	ERR4552431_2.fastq.gz	Fastqsanger.gz
	ERR4552432_1.fastq.gz	Fastqsanger.gz

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RNA-seq of Zbtb10 Knockdown and Control cDC1 dendritic cells (Cd8+)

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CD8 T cells are primed by cDC1 and exacerbate tau-mediated neurodegeneration

Project description:There are changes in adaptive immunity in Alzheimer’s disease (AD) and increases in activated CD8 T cells in brain correlate with tau pathology. However, which cells mediate T cell priming in tau-mediated neurodegeneration remains unclear. In different conditions such as cancer, viral infections, and autoimmune diseases outside the CNS, conventional type-1 dendritic cells (cDC1) perform antigen cross-presentation to prime CD8 T cells. We demonstrate that tauopathy mice deficient in cDC1 are markedly protected against tau-mediated neurodegeneration and display a selective decrease in brain CD8 T cell infiltration and glial reactivity. The remaining CD8 T cells showed an antigen inexperienced status with less clonal expansion, indicating suboptimal T cell priming. We confirm that brain derived antigens are presented in the secondary lymphoid tissues to prime CD8 T cells. Our study identifies cDC1 as critical for CD8 T cell priming outside of the CNS. This priming is required for a large increase in activated CD8 T cells in the brain which promotes tau-mediated neurodegeneration.

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E-MTAB-9495

Project description:RNA-seq of Zbtb10 Knockdown and Control cDC1 dendritic cells (Cd8+)

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CD8+ T cells are primed by cDC1 and exacerbate tau-mediated neurodegeneration

Project description:There are changes in adaptive immunity in Alzheimer’s disease (AD) and increases in activated CD8+ T cells in brain correlate with tau pathology. However, which cells mediate T cell priming in tau-mediated neurodegeneration remains unclear. In different conditions such as cancer, viral infections, and autoimmune diseases outside the CNS, conventional type-1 dendritic cells (cDC1) perform antigen cross-presentation to prime CD8+ T cells4,5. We demonstrate that tauopathy mice deficient in cDC1 or cross-presentation are markedly protected against tau-mediated neurodegeneration and display a selective decrease in brain CD8+ T cell infiltration and glial reactivity. The remaining CD8+ T cells showed an antigen inexperienced status with less clonal expansion, indicating suboptimal T cell priming. We confirm that brain derived antigens are presented in secondary lymphoid tissues to prime CD8+ T cells. Our study identifies cDC1 cells as critical for CD8+ T cell priming outside the CNS. This priming is required for a large increase of activated CD8+ T cells in the brain which promotes tau-mediated neurodegeneration.

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