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BCR and TLR-induced IRF1 promotes T cell independent B cell responses by supporting Notch2 dependent Marginal Zone B cell development

ABSTRACT: BCR and TLR-induced IRF1 promotes T cell independent B cell responses by supporting Notch2 dependent Marginal Zone B cell development

PROVIDER: PRJNA1046020 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26978371_1.fastq.gz	Fastqsanger.gz
	SRR26978371_2.fastq.gz	Fastqsanger.gz
	SRR26978372_1.fastq.gz	Fastqsanger.gz
	SRR26978372_2.fastq.gz	Fastqsanger.gz
	SRR26978373_1.fastq.gz	Fastqsanger.gz

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BCR and TLR-induced IRF1 promotes T cell independent B cell responses by supporting Notch2 dependent Marginal Zone B cell development

Project description:The prototypic interferon (IFN)-inducible transcription factor, IRF1, not only controls expression of IFN genes but also regulates T cell and macrophage fate specification and function. We show that IRF1 expression in B cells is required for marginal zone B (MZB) cell development and T cell independent antibody responses [80% B6.129S2-Ighmtm1Cgn/J (MT) + B6.129S2-Irf1tm1Mak/J (Irf1-/-), B-Irf1-/- chimeras]. While IFNs can induce IRF1 expression in MZB precursors, IFN signaling is not required for MZB cell development [C57BL/6J (B6), B6.129S7-Ifngr1tm1Agt/J (Ifngr1-/-), B6(Cg)-Ifnar1tm1Agt/J (Ifnar1-/-)]. Instead, BCR and TLR signals, which influence MZB commitment, promote IRF1 expression and nuclear translocation in MZB cell precursors. In turn, IRF1 is required for Notch-dependent gene expression in transitional B cells and development of the MZB cell compartment. Thus, T independent MZB-driven antibody responses are regulated by BCR and TLR signals that initiate IRF1-dependent Notch programming of transitional B cells and subsequent commitment of these cells to the MZB lineage.

2024-11-01 | GSE248790 | GEO

Notch and TLR signaling coordinate monocyte cell fate and inflammation

Project description:We studied the role of Notch2 signaling in Ly6Chi monocyte cell fate during TLR7-induced acute inflammation. To characterize the gene expression changes involved in monocyte differentiation, we subjected monocyte subsets from peripheral blood of wt and myeloid Notch2 mutant mice after Sham or IMQ treatment to RNA-sequencing and gene expression analysis. We found that Cell-intrinsic Notch2 and TLR7-Myd88 pathways independently and synergistically promote Ly6Clo patrolling monocyte development from Ly6Chi monocytes under inflammatory conditions. At the same time TLR7 stimulation in the absence of functional Notch2 signaling promotes resident tissue macrophage gene expression signatures in monocytes and ectopic differentiation of Ly6Chi monocytes into macrophages and dendritic cells. Thus, Notch2 is a master regulator of Ly6Chi monocyte cell fate and inflammation in response to TLR signaling.

2020-08-04 | GSE147492 | 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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Identification of Myc-dependent and -independent Notch2 signatures in marginal zone B cells.

Project description:Marginal zone (MZ) B cells leverage Notch2 signals to attain rapid differentiation responses and positional cues with in the spenic environment. While it is known that a major player in Notch2 signaling in MZ B cells is the proto-oncogene Myc, it is not clear to what extent MZ B cells use Notch2 signals in Myc-independent manner. In this study we conditinally and inducibly deleted Myc in mature B cells and then used in vivo delivery of anti-Notch2 antibodies to separated Myc-dependent and -independent Notch2 signaling in MZ B cells.

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Transcriptomic analyis follicular and marginal zone B ells after in vivo Notch2 blockade.

Project description:Marginal zone B cells which make rapid mitosis-independent plasma cell responses are dependent on Notch2 signaling for their generation and maintenance. In order to determine the effect of ongoing Notch signaling on the maintenance of the MZ transcriptome, we performed RNA-seq on MZ and follicular B cells after 12, 24 and 48 hours of in vivo Notch2 antibody blockade

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Marginal zone B cells receive robust Notch2 signals within the B cell follicle in the absense of S1pr1 signaling.

Project description:Marginal zone (MZ) B cells have innate-like response characteristics due to a unique ability receive and integrate Notch2 signals in the spleen. There is evidence showing MZ B cells receive these signals both in the marginal sinus and the B cell follicle. The relative strength and conservation of these Notch signals is not yet clear. Therefore, we generated mice in which S1pr1 is deleted in mature B cells. These mice have MZ B cells by phenotype but these cells are retained in the follicle and unable to transit to the marginal zone. In this experiment we examined the impact of Notch2 signaling in these cells and cre expressing control animals using in vivo anti-Notch2 antibody blockade followed by RNA-sequencing.

2024-10-18 | GSE274990 | GEO

NOTCH2 mutants

Project description:NOTCH2 mutants

| PRJNA967022 | ENA

IRF1 governs the differential Interferon-Stimulated Gene responses in human monocytes and macrophages by regulating chromatin accessibility (ATAC - IRF1 KO THP-1)

2021-03-16 | GSE147308 | GEO

Notch2 over expression in urinary bladder RT4V6 cell line

Project description:Notch2 in promotion of bladder cancer growth and metastasis through epithelial to mesenchymal transition (EMT), cell cycle progression and maintenance of stemness. Notch2 induced gene expression in human urinary bladder cancer was measured at three independent experiments.

2014-08-21 | E-GEOD-60564 | biostudies-arrayexpress

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