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Bulk RNA-seq analysis of Mycobacterium tuberculosis infected Sp140-sufficient and -deficient mouse lungs with and without pDC depletion

ABSTRACT: Bulk RNA-seq analysis of Mycobacterium tuberculosis infected Sp140-sufficient and -deficient mouse lungs with and without pDC depletion

PROVIDER: PRJNA974429 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24660400_1.fastq.gz	Fastqsanger.gz
	SRR24660400_2.fastq.gz	Fastqsanger.gz
	SRR24660401_1.fastq.gz	Fastqsanger.gz
	SRR24660401_2.fastq.gz	Fastqsanger.gz
	SRR24660402_1.fastq.gz	Fastqsanger.gz

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Bulk RNA-seq analysis of Mycobacterium tuberculosis infected Sp140-sufficient and -deficient mouse lungs with and without pDC depletion

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.

2024-01-12 | GSE232922 | GEO

Sp140 interactome analysis and proteomic analyis of WT vs Sp140 KO in Burkitt lynphoma

Project description:Interactomic anaysis of Sp140 in Burkitt lynphoma and proteomic analyis of WT vs Sp140 KO in Ramos cell line

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

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

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Gene expression analysis of E16.5 Stk11-sufficient control and Sk11-/- lungs

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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.

2024-06-18 | GSE266432 | GEO

Immune-restricted epigenetic reader SP140 maintains macrophage identity and activation states critical to intestinal homeostasis [array]

Project description:Introduction: SP140 is a bromodomain/plant homeo domain (PHD)-containing reader with immune-restricted expression, and single nucleotide polymorphisms (SNPs) within SP140 associate with Crohn’s disease (CD). However, the function of SP140 and the consequences of disease-associated SP140 SNPs have remained unknown. Results: Individuals carrying CD-associated SNPs within SP140 had defective SP140 mRNA splicing, diminished SP140 protein, and severely suppressed innate immune signatures that stratified them from other CD patients. Conclusion: SP140 is a critical orchestrator of macrophage identity, and a loss of SP140 due to genetic variation contributes to a molecularly defined subset of CD characterized by suppressed innate immunity.

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Immune-restricted epigenetic reader SP140 maintains macrophage identity and activation states critical to intestinal homeostasis [ChIP-seq]

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Immune-restricted epigenetic reader SP140 maintains macrophage identity and activation states critical to intestinal homeostasis [ATAC-Seq]

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Immune-restricted epigenetic reader SP140 maintains macrophage identity and activation states critical to intestinal homeostasis [RNA-seq]

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Transcriptional repression of IRF7 by MYC is critical for antiviral immune response in human pDC [pDC]

Project description:Type I interferons (IFN) are crucial mediators of human innate and adaptive immunity and are massively produced from plasmacytoid dendritic cells (pDC). IRF7 is a critical regulator of type I IFN production when pathogens are detected by TLR7/9 in pDC. However, hyperactivation of pDC can cause life-threatening autoimmune diseases. To avoid the deleterious effects of aberrant pDC activation, tight regulation of IRF7 is required. Nonetheless, the detailed mechanisms of how IRF7 transcription is regulated in pDC are still elusive. To this end, we identified the global gene expression changes after stimulation of human primary pDC with the TLR9 agonist CpGB. We identified that the transcription factor MYC is prominently upregulated upon CpGB engagement in pDC. Moreover, when we knocked down MYC in the pDC-like cell line GEN2.2, production of interferon-stimulated genes (ISGs) was dramatically increased and was further enhanced by CpGB. Interestingly, MYC is shown to be recruited to the IRF7 promoter region through interaction with NCOR2/HDAC3 for its repression, and HDAC3 inhibition enhanced IRF7 expression and IFNβ production. Interestingly, activation of TLR9-mediated NF-kB and MAPK and nuclear translocation of IRF7 were greatly enhanced by MYC depletion. Pharmaceutical inhibition of MYC recovered IRF7 expression, further confirming the negative role of MYC in the antiviral response by pDC. Furthermore, the inverse correlation of MYC and IRF7 was validated in psoriasis skin sample datasets. Therefore, our results identify the novel immunomodulatory role of MYC in human pDC and may add to our understanding of aberrant pDC function in autoimmune diseases.

2018-06-01 | GSE70277 | GEO

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