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CXCR4 drives lympho-myeloid fate of hematopoietic progenitors via mTOR and mitochondrial metabolic pathways

ABSTRACT: CXCR4 drives lympho-myeloid fate of hematopoietic progenitors via mTOR and mitochondrial metabolic pathways

PROVIDER: PRJNA758688 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15663600_1.fastq.gz	Fastqsanger.gz
	SRR15663600_2.fastq.gz	Fastqsanger.gz
	SRR15663601_1.fastq.gz	Fastqsanger.gz
	SRR15663601_2.fastq.gz	Fastqsanger.gz
	SRR15663602_1.fastq.gz	Fastqsanger.gz

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CXCR4 drives lympho-myeloid fate of hematopoietic progenitors via mTOR and mitochondrial metabolic pathways

Project description:Hematopoietic stem and progenitor cells (HSPCs), including the multipotent progenitors (MPPs), are responsible for replenishing immune cells. They reside in bone marrow (BM) endosteal and (peri)-vascular niches, which provide all cellular and molecular components required for their lifelong maintenance and fate. Among them, the CXCL12 chemokine and one of its receptor, CXCR4, exert a dominant role in promoting HSPC retention and quiescence. These processes are deregulated in the WHIM Syndrome (WS), a rare immunodeficiency caused by inherited heterozygous autosomal gain-of-function CXCR4 mutations that affect homologous desensitization of the receptor. Clinically, WS is notably characterized by severe, chronic circulating lymphopenia whose mechanisms remain to be elucidated. Using a mouse model carrying a naturally occurring WS-linked Cxcr4 mutation, we explored the possibility that the lymphopenia in WS originates from defects at the MPP level in BM. The global strategy consists in performing high-throughput RNA-seq analyses of the different MPP subsets bearing or not the WS-linked Cxcr4 mutation to investigate the impact of the gain-of-Cxcr4-function on the molecular identity of MPP subsets.

2021-09-02 | GSE182992 | GEO

Non-apoptotic Fas signaling controls CD40 dependent mTOR activation and human B cell fate via PTEN nuclear exclusion

Project description:Defective Fas signaling causes autoimmune lymphoproliferative syndrome (ALPS). While defective apoptosis may impair negative selection and removal of autoreactive B lymphocytes, Fas transmits also non-apoptotic signals. We show herethat transient Fas ligation in CD40L-stimulated human B cells specifically decreased the mTOR axis activation without causing apoptosis. This signal modulation was absent in ALPS patients. Rather, mTOR signaling was enhanced in germinal center (GC) B cells and plasmablasts derived from a ALPS patient lymph node . Mechanistically, transient Fas engagement induced recruitment of DAXX to the activated Fas complex and nuclear exclusion of PTEN. Likewise, Fas stimulation promoted expression of transcripts like MYC and CXCR4, that regulate GC formation and fate decisions of established GC B cells. We suggest that non-apoptotic Fas signaling has a physiological impact on activated B cell fate decisions explaining the effectiveness of mTOR inhibitors in the treatment of ALPS autoimmunity.

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EBF1 contributes to the balance of lympho-myeloid fate in haematopoietic progenitors via B-lymphoid priming and Cebpa antagonism

Project description:EBF1 contributes to the balance of lympho-myeloid fate in haematopoietic progenitors via B-lymphoid priming and Cebpa antagonism

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EBF1 contributes to the balance of lympho-myeloid fate in haematopoietic progenitors via B-lymphoid priming and Cebpa antagonism [10x]

Project description:EBF1 contributes to the balance of lympho-myeloid fate in haematopoietic progenitors via B-lymphoid priming and Cebpa antagonism [10x]

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EBF1 contributes to the balance of lympho-myeloid fate in haematopoietic progenitors via B-lymphoid priming and Cebpa antagonism [ATAC-seq]

Project description:EBF1 contributes to the balance of lympho-myeloid fate in haematopoietic progenitors via B-lymphoid priming and Cebpa antagonism [ATAC-seq]

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EBF1 contributes to the balance of lympho-myeloid fate in haematopoietic progenitors via B-lymphoid priming and Cebpa antagonism [Bulk RNA-seq]

Project description:EBF1 contributes to the balance of lympho-myeloid fate in haematopoietic progenitors via B-lymphoid priming and Cebpa antagonism [Bulk RNA-seq]

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Developmentally controlled expression of Cxcr4 by hematopoietic progenitors allows tracing of monocyte function in stroke

Project description:Monocyte-derived and tissue-resident macrophages, such as microglia, belong to independent lineages with distinct functions in steady state. During inflammation, however, changes in phenotypes and transcriptional profiles make it difficult to assess their respective roles in pathology. Here, we report that developmentally controlled expression of Cxcr4 by hematopoietic progenitors allows highly specific inducible lineage tracing of hematopoietic stem cell-derived monocytes during inflammation. In two stroke models, we found that monocytes recruited to the brain were confined to the lesion and its surrounding during the acute phase. However, monocytes did not engraft in peri-lesional tissue, but were enclosed in scar tissue by microglia and astrocytes after completed repair. Transcriptional profiles of brain monocytes and microglia reflect major differences in signaling pathways, paracrine mediators, and proliferative behavior. Initial recruitment and subsequent enclosure of monocytes required Cxcr4. Our data show that CXCR4 signaling regulates a specific monocyte-mediated contribution to injury and repair in stroke.

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