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Gene expression profile at single cell level of monocytes (MOs) and T cells from the lungs and from broncho-alveolar lavage fluids (BALF) from Mock and MuHV-4 infected WT and CCR2 KO mice.

ABSTRACT: Gene expression profile at single cell level of monocytes (MOs) and T cells from the lungs and from broncho-alveolar lavage fluids (BALF) from Mock and MuHV-4 infected WT and CCR2 KO mice.

PROVIDER: PRJNA848239 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19631855.fastq.gz	Fastqsanger.gz
	SRR19631856.fastq.gz	Fastqsanger.gz
	SRR19631857_1.fastq.gz	Fastqsanger.gz
	SRR19631857_2.fastq.gz	Fastqsanger.gz
	SRR19631858_1.fastq.gz	Fastqsanger.gz

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Gene expression profile at single cell level of monocytes (MOs) and T cells from the lungs and from broncho-alveolar lavage fluids (BALF) from Mock and MuHV-4 infected WT and CCR2 KO mice.

Project description:Gammaherpesviruses (γHVs) have co-evolved with their hosts over millions of years, leading to remarkably high infection prevalence and establishment of symbiotic relationship. Therefore, the lifelong persistence of γHVs appear to broadly shape host immunity. Here, we show that pulmonary infection with Murid herpesvirus 4 (MuHV-4), a mouse γHV, drives the recruitment in the airways of Ly6Chi monocytes (MOs) that control the host immune response. Indeed, the absence of those MOs elicits a severe virus-induced immunopathology associated with the systemic release of inflammatory mediators. Mechanistically, MuHV-4 imprinted MOs recruit CD4 T cells in the airways and trigger immunosuppressive signalling pathways through the PDL1/PD-1 axis, thereby dampening the deleterious activation of cytotoxic CD4 T cells. These results uncover a role for Ly6Chi MOs in the modulation of CD4 T cell functions, and reveal key pathways that could be targeted to interfere with the detrimental immunopathological cascade during respiratory viral infections.

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CCR2+ vs. CCR2- murine hematopoietic stem cells

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Disrupted MOS signaling alters meiotic cell cycle regulation and the egg transcriptome

Project description:Loss of MOS in female mice disrupts metaphase II arrest, potentially causing infertility and germ cell tumors. Single-egg RNA sequencing revealed widespread gene expression changes in mos -/- eggs, including upregulation of cell cycle regulators like Aurka, Bub3, and Cdk7. Pathways related to RNA metabolism, transcription, and neddylation were also enriched in mos -/- eggs. Notably, the transcriptome of mos -/- eggs differed from that of chemically activated eggs. These results highlight MOS as a key regulator of the meiotic cell cycle and transcriptome integrity essential for oocyte developmental competence.

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Transcriptome comparison between CCR2+ and CCR2- classical monocytes in SIV-infected Macaca nemestrina

Project description:Monocytes have been categorized in three main subpopulations based on CD14 and CD16 surface expression. Classical monocytes are the most abundant subset in the blood. They express a CD14+CD16-CCR2+ phenotype, which confers on them the ability to migrate to inflammatory sites by quickly responding to CCL2 signaling. Here we identified and characterized the surge and expansion of a novel monocyte subset during SIV and HIV infection. They were undistinguishable from classical monocytes regarding CD14 and CD16 expression, but did not express surface CCR2. Transcriptome analysis of sorted cells confirmed that they represent a distinct subpopulation that expresses lower levels of inflammatory cytokines and activation markers than their CCR2+ counterparts. They exhibited impaired phagocytosis and deficient chemotaxis in response to CCL2 and CCL7, besides being refractory to SIV infection. We named these cells atypical CCR2- classical (ACC) monocytes, and believe they play an important role in AIDS pathogenesis, possibly reflecting an anti-inflammatory response against the extreme immune activation observed during SIV and HIV infection. Antiretroviral therapy caused this population to decline in both macaque and human subjects, suggesting that this atypical phenotype may be induced by viral replication. Expression profiling by NanoString nCounter gene expression system. Classical monocytes (CD14++CD16-) from six SIV-infected macaques (day 14 post inoculation) were sorted in two groups according to CCR2 expression.

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Phosphoproteomics identifies targets of Mos-MAPK regulating translation and spindle organization in oocyte meiosis

Project description:The Mos kinase is a constitutive activator of the ERK/MAPK pathway exclusively expressed during oocyte meiosis, mediating key meiotic functions across animal species. While a few of its downstream effectors have been studied in some detail, molecular targets under the control of Mos-MAPK have not yet been identified systematically. Here, we combined live-cell microscopy of starfish oocytes to characterize the cellular phenotypes caused by Mos-MAPK inhibition with phosphoproteomic analysis of synchronous oocyte populations at critical transitions. This revealed a large set of proteins involved in regulation of translation through the CPE-element binding protein CPEB. Our data indicate cyclin B to be a main target of this regulation driving the second meiotic division. A second large group of phospho-proteins identified are regulators of the actin and microtubule cytoskeleton, with a prominent subset of regulators of centrosomal microtubule nucleation. Indeed, we show that Mos-MAPK inhibition increases the size of microtubule asters and promotes separation of spindle poles in anaphase, turning meiotic spindles mitotic-like. We thus identified core molecular modules downstream of Mos-MAPK controlling meiotic functions essential for haploidization and for the highly asymmetric polar body divisions. These modules are widely conserved, thus our findings will likely have general relevance for reproductive processes across species, including humans, and for understanding disease mechanisms when Mos is expressed erroneously, acting as an oncogene.

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Broncho brushing samples from healthy donors and Job's Syndrome patients

Project description:To find the DEGs between healthy donors and Job's Syndrome patients, we extracted RNA from broncho brushing samples collected from healthy donors and Job's Syndrome patients.

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Phosphoproteomic Characterization of Signaling Networks Resulting from Activation of Chemokine Receptor CCR2

Project description:Leukocyte recruitment, a universal feature of tissue inflammation, is regulated by the interactions of chemokines with their G protein-coupled receptors. Activation of CC chemokine receptor 2 (CCR2) by its cognate chemokine ligands, including CCL2, plays a central role in recruitment of monocytes in several inflammatory diseases. In this study, we used phosphoproteomics to enable unbiased characterization of the signaling network resulting from CCL2 activation of CCR2. Using data-independent acquisition (DIA) mass spectrometry, both the proteome and phosphoproteome were quantified for FlpIn-HEK293T cells stably expressing CCR2, at six time points after activation with CCL2, in comparison with untreated cells. Differential expression analysis identified 699 significantly regulated phosphorylation sites located on 441 proteins. As expected, many of these proteins participate in canonical signal transduction pathways and the regulation of actin cytoskeleton dynamics, including numerous guanine nucleotide exchange factors (GEFs) and GTPase activating proteins (GAPs). In addition, we identified regulated phosphorylation sites in numerous proteins that exert functions in the nucleus, including several constituents of the nuclear pore complex. This study provides an unprecedented level of detail about CCR2 signalling and identifies potential novel targets for regulation of CCR2 function.

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