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CITE-seq analysis of Mycobacterium tuberculosis infected B6 and Sp140-deficient mouse lungs

ABSTRACT: CITE-seq analysis of Mycobacterium tuberculosis infected B6 and Sp140-deficient mouse lungs

PROVIDER: PRJNA891725 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21953939.fastq.gz	Fastqsanger.gz
	SRR21953940.fastq.gz	Fastqsanger.gz
	SRR21953941.fastq.gz	Fastqsanger.gz
	SRR21953942.fastq.gz	Fastqsanger.gz
	SRR21953943.fastq.gz	Fastqsanger.gz

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CoMtb alters the immune landscape following Mtb infection [B6 Sp140-/- scRNA-Seq]

Project description:To gain further insights into lesion development and effects of CoMtb on immune responses during infection. we performed single-cell RNA sequencing (scRNAseq) and flow cytometry analysis of lungs from Mtb-infected B6 Sp140-/- mice with and without CoMtb at 10 days after CD infection. We found that CoMtb induces rapid recruitment and activation of T cells. macrophage activation. and diminished late neutrophil responses.

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CITE-seq analysis of Mycobacterium tuberculosis infected B6 and Sp140-deficient mouse lungs

Project description:Mycobacterium tuberculosis (Mtb) causes 1.5 million deaths annually. Active tuberculosis correlates with a neutrophil-driven type I interferon (IFN) signature, but the underlying cellular mechanisms remain poorly understood. We found that interstitial macrophages (IMs) and plasmacytoid dendritic cells (pDCs) are dominant producers of type I IFN during Mtb infection in mice and non-human primates, and pDCs localize near human Mtb granulomas. Depletion of pDCs reduces Mtb burdens, implicating pDCs in tuberculosis pathogenesis. During IFN-driven disease, we observe abundant DNA-containing neutrophil extracellular traps (NETs) known to activate pDCs. Single cell RNA-seq indicates that type I IFNs act on IMs to impair their responses to IFNg, a cytokine critical for Mtb control. Cell type-specific disruption of the type I IFN receptor suggests IFNs act on IMs to inhibit Mtb control. We propose pDC-derived type I IFNs, driven by NETs, act on IMs to drive bacterial replication, further neutrophil recruitment, and active tuberculosis disease.

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The antiviral nuclear body protein SP140 represses Ifnb1 transcript stabilization by the novel regulator RESIST [WT and SP140 KO RNA-seq]

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CoMtb alters the immune landscape following Mtb infection [B6 Sp140-/- scRNA-Seq]

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