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Comparison of Ly6c high splenic monocytes from IL-17A/F-deficient versus control mice

ABSTRACT: Comparison of Ly6c high splenic monocytes from IL-17A/F-deficient versus control mice

PROVIDER: PRJNA542872 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9054151_1.fastq.gz	Fastqsanger.gz
	SRR9054151_2.fastq.gz	Fastqsanger.gz

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Comparison of Ly6c high splenic monocytes from IL-17A/F-deficient versus control mice

Project description:The goal of this study was to compare transcriptional changes, on the single cell level, in splenic monocytes evoked by global IL-17A/F deficiency

2020-05-08 | GSE131183 | GEO

AffyExon1 genearray expression profile of adult mouse microglia and splenic Ly6C monocytes

Project description:Gene profiling of CNS-derived microglia vs splenic CD11b+Ly6C+ monocyte subsets deom adult mice Gene array identified 1572 genes that were enriched in microglia vs. 611 monocyte enriched genes with a greater than 5-fold difference (P<0.001). Gene profiling of CD11b+CD45Low microglia isolated from the CNS and CD11b+Ly6C+ monocyte subsets isolated from the spleen of naM-CM-/ve adult mice.

2013-07-08 | E-GEOD-48579 | biostudies-arrayexpress

Genomic characterization of murine monocytes reveals C/EBPb dependence of Ly6C-cells [RNA sequence]

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2017-05-15 | GSE95411 | GEO

Genomic characterization of murine monocytes reveals C/EBPb dependence of Ly6C-cells [ChIP data]

Project description:Chromatin status of murine blood Ly6C+ and Ly6C- monocytes indicates that both population share K4me3 marks (promoters) while Ly6C- monocytes establish de novo enhancers (K4me1, K4me2) during differentiation

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G-CSF mobilizes CD34+ regulatory monocytes that inhibit Graft-versus-Host Disease

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The Expression profile of splenic Ly6C low/Ly6C high macrophages in SLC29A3 deficient mice

Project description:Loss-of-function mutations in the lysosomal nucleoside transporter SLC29A3 lead to the accumulation of nucleosides in lysosomes and result in histiocytosis, characterized by the excessive accumulation of phagocytes in multiple organs. However, the underlying mechanism by which lysosomal nucleoside storage drives histiocytosis remains poorly understood. Herein, we provide evidence that histiocytosis in Slc29a3–/– mice is dependent on Toll-like receptor 7 (TLR7), which senses a combination of guanosines and oligoribonucleotides. TLR7 increased phagocyte populations by driving the proliferation of immature Ly6C high splenic macrophages and their subsequent maturation into Ly6C low phagocytes in Slc29a3–/– mice. Interestingly, TLR7 activation in nucleoside-laden splenic macrophages failed to induce inflammatory responses. Our data demonstrate that TLR7 responses to lysosomal nucleoside stress drive unique immune responses distinct from inflammation in SLC29A3-related disorders.

2023-06-17 | GSE234367 | GEO

G-CSF mobilizes CD34+ regulatory monocytes that inhibit Graft-versus-Host Disease

Project description:Administration of G-CSF mobilizes a unique population of CD11b+Ly6C+CD34+mature monocytes that can inhibit GVHD in murine models of BMT via an iNOS-dependent mechanism. The transcriptional profiles of flow sorted lineage-CD11b+CD34+ cells from G-CSF treated mice were compared with conventional splenic Ly6C+ and Ly6C- monocytes, progenitor cells and cultured myeloid-derived suppressor cells. Further comparisons were made with lineage-CD11b+CD34+ cells from G-CSF treated mice that had been grown in culture or that were derived from iNOS ko mice. We used microarrays to detail the global programme of gene expression underlying diffrenetiation of each of these cell types Lin-CD11b+CD34+ populations were isolated directly from the spleens of G-CSF-treated C57BL/6 mice or iNOS ko mice. In untreated C57BL/6 mice, Lin-CD11b+CD115+Ly6C+ and Lin-CD11b+CD115+Ly6C- monocytes were isolated from the spleen and Lin-CD117+CD115+CD135-Ly6C+CD11b- common monocyte progenitors were isolated from the bone marrow. Myeloid-derived suppressor cells (Ly6C+CD11b+ cells derived from G-CSF, GM-CSF and IL-13 cultured C57BL/6 bone marrow) were also isolated and compared with the above populations. Lin-CD11b+CD34+ spleen cells derived from G-CSF-treated C57BL/6 mice were cultured for 3 days in Flt3 ligand and SCF and then compared to the original input population.

2015-04-01 | E-GEOD-65670 | biostudies-arrayexpress

The Expression profile of splenic Ly6C low/Ly6C high macrophages in SLC29A3 deficient mice

Project description:The Expression profile of splenic Ly6C low/Ly6C high macrophages in SLC29A3 deficient mice

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Expression data from mouse circulating Ly6C-low subset of monocytes (patrolling monocytes)

Project description:Expression data from mouse circulating Ly6C-low subset of monocytes (patrolling monocytes)

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Expression arrays of inflammatory Ly6C+ monocytes in mice primary or secondary challenged with Listeria monocytogenes

Project description:In this study we investigated the mechanisms involved in memory T-cell mediated protection using mice vaccinated with the intracellular bacterium Listeria monocytogenes. Our working hypothesis was that rapid activation of cells of the innate immune system, in particular inflammatory Ly6C+ monocytes, were essential in effective protection, in a memory T cell-dependent manner. Thus we generated a comprehensive comparison of the genetic program of activated Ly6C+ monocytes during a primary or a secondary infection with Listeria monocytogenes, at 8 hours post challenge infection. Abstract of corresponding publication: Cells of the innate immune system are essential for host defenses against primary microbial pathogen infections, yet their involvement in effective memory responses of vaccinated individuals has been poorly investigated. Here we show that memory T cells instruct innate cells to become potent effector cells in a systemic and a mucosal model of infection. Memory T cells controlled phagocyte, dendritic cell and NK or NK T cell mobilization and induction of a strong program of differentiation, which included their expression of effector cytokines and microbicidal pathways, all of which were delayed in non-vaccinated hosts. Disruption of IFN-gamma-signaling in Ly6C+ monocytes, dendritic cells and macrophages impaired these processes and the control of pathogen growth. These results reveal how memory T cells, through rapid secretion of IFN-gamma, orchestrate extensive modifications of host innate immune responses that are essential for effective protection of vaccinated hosts. Overall design: Inflammatory monocytes were purified (see below for isolation method) from 4 groups of 3 individual mice each (triplicate): (i) uninfected mice, (ii) primary infected, (iii) secondary infected, (iv) secondary infected and T-cell depleted 1 day before. Isolation of cells was done on 3 different days for true biological replicates.

2015-06-04 | E-GEOD-58014 | biostudies-arrayexpress

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