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Transcriptional analysis of dendritic cells upon TLR stimulation reveals an immunosuppressive profile [cut&tag]

ABSTRACT: Transcriptional analysis of dendritic cells upon TLR stimulation reveals an immunosuppressive profile [cut&tag]

PROVIDER: PRJNA1083872 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28227817_1.fastq.gz	Fastqsanger.gz
	SRR28227817_2.fastq.gz	Fastqsanger.gz
	SRR28227818_1.fastq.gz	Fastqsanger.gz
	SRR28227818_2.fastq.gz	Fastqsanger.gz
	SRR28227819_1.fastq.gz	Fastqsanger.gz

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Transcriptional analysis of dendritic cells upon TLR stimulation reveals an immunosuppressive profile [PLF scRNA-seq]

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Transcriptional analysis of dendritic cells upon TLR stimulation reveals an immunosuppressive profile [PBMC scRNA-seq]

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Transcriptional analysis of dendritic cells upon TLR stimulation reveals an immunosuppressive profile [cut&tag]

Project description:Dendritic cells (DCs) simultaneously prime and dampen the immune response. The transcriptional program that regulates immunosuppression in DCs is currently unknown. Here we identified ETS homologous factor as a key transcription factor that regulates DC immunosuppression.

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Transcriptional analysis of dendritic cells upon TLR stimulation reveals an immunosuppressive profile [PBMC scRNA-seq]

2025-03-01 | GSE260860 | GEO

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2025-03-01 | GSE260857 | GEO

IRF1 governs the differential Interferon-Stimulated Gene responses in human monocytes and macrophages by regulating chromatin accessibility (RNA-seq - TLR stimulation)

Project description:Myeloid lineage cells use TLRs to recognize and respond to diverse microbial ligands. Although unique transcription factors dictate the outcome of specific TLR signaling, whether lineage-specific differences exist to further modulate the quality of TLR-induced inflammation remains unclear. Comprehensive analysis of global gene transcription in human monocytes, monocyte-derived macrophages and monocyte-derived dendritic cells stimulated with various TLR ligands identifies multiple lineage-specific, TLR-responsive gene programs. Monocytes are hyperresponsive to TLR7/8 stimulation that correlates with higher expression of the receptors. While macrophages and monocytes express similar levels of TLR4, macrophages, but not monocytes, upregulate Interferon-Stimulated Genes (ISGs) in response to TLR4 stimulation. We find that TLR4 signaling in macrophages uniquely engages transcription factor IRF1, which facilitates opening of ISG loci for transcription. This study provides a critical mechanistic basis for lineage-specific TLR responses and uncovers IRF1 as a master epigenetic regulator for the ISG transcriptional program in human macrophages.

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