Expression data from mouse spleen pre-Red Pulp Macrophages (PreRPM), circulating Ly6C-low subset of monocytes (patrolling monocytes), and bone marrow derived macrophages (BMDM)
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PROVIDER: PRJNA632623 | ENA |
REPOSITORIES: ENA
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Project description:Expression data from mouse circulating Ly6C-low subset of monocytes (patrolling monocytes)
| PRJNA632620 | ENA
Project description:The transcription factor Spic regulates genes associated with heme and iron metabolism. We used microarrays to identify genes regulated by the transcription factor Spic in patrolling monocytes.
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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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Project description:Lung interstitium macrophages (IMs) are non-alveolar resident tissue macrophages which contribute to the lung homeostasis. These cells were reported to be heterogeneous by our group and other teams, which contains two main distinct subpopulations: CD206+ IMs and CD206- IMs. However, the exact origin of IMs and the transcriptional programs that regulate IM differentiation remains unclear. In recent report, we analyzed the refilled IMs in the course of time after induced IM depletion with single-cell RNA sequencing (10X Genomics Chromium) and bulk RNA sequencing. The lung IMs and monocytes from either Lyz2-Cre Mafflox/flox mice (cMAF-KO), Lyz2-Cre Mafbflox/flox (MAFb-KO), Lyz2-Cre Mafflox/flox Mafbflox/flox (dKO) or control litermate mice without floxp locus (Control) were analyzed and compared using single-cell RNA sequencing. All the main substs, i.e. Ly6C+ classical monocytes, Ly6C- patrolling monocytes, CD206+ IMs, CD206- IMs were found in control sample, while IMs are absent in both MAFb-KO and dKO sample accompied by a new intermediate population independent of Mafb expression. CMAF-KO sample show less impact in cell population composition with a lower freqency of CD206+ IM population.
2023-02-07 | GSE193891 | GEO
Project description:Splenic red pulp macrophages (RPM) degrade senescent erythrocytes and recycle heme-associated iron. The transcription factor Spic is selectively expressed by RPM and is required for their development, but the physiologic stimulus inducing Spic is unknown. Here, we report that Spic also regulated the development of F4/80+VCAM+ bone marrow macrophages (BMM) and that Spic expression in BMM and RPM development was induced by heme, a metabolite of erythrocyte degradation. Pathologic hemolysis induced loss of RPM and BMM due to excess heme but induced Spic in monocytes to generate new RPM and BMM. Spic expression in monocytes was constitutively inhibited by the transcriptional repressor Bach1. Heme induced proteasome-dependent BACH1 degradation and rapid Spic derepression. Further, cysteine-proline dipeptide motifs in BACH1 that mediate heme-dependent degradation were necessary for Spic induction by heme. These findings are the first example of metabolite-driven differentiation of a tissue-resident macrophage subset and provide new insight into iron homeostasis. Global gene expression pattern of Spic+ monocytes, Spic- monocytes, and Spic high red pulp macrophages were compared by sorting these cells from Spic(igfp/+) splenocytes and performing microarray-based gene expression profiling. Splenocytes were prepared from Spic(igfp/+) mice and were first negatively selected for CD4, CD8, and B220 by MACS (Miltenyi Biotech) purification using the respective microbeads. Negatively selected splenocytes were then stained with anti-CD11b and anti-Ly6c and sorted for Spic+ monocytes (CD11b+Ly6c+Spic+) and Spic- monocytes (CD11b+Ly6c+Spic-). Purified RPM were obtained by staining splenocytes with anti-F4/80 and sorting for F4/80 hi Spic-EGFP hi cells.
2014-03-14 | E-GEOD-46984 | biostudies-arrayexpress
Project description:Gene expression in Lung digest CD64hiSiglecF-Ly6C-MHC- macrophages from PBS-treated mice and CD64hiSiglecF-Ly6C-MHC-Lyve1+ macrophages, assayed on NanoString nCounter Mouse Myeloid Innate Immunity Panel panel (GPL30135) Nanostring expression data
2022-06-23 | GSE200558 | GEO
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
Project description:We sought to evaluate in an unbiased way the heterogeneity of lung interstitial macrophages and their relationship with alveolar macrophages, lung Ly-6Chi classical monocytes and Ly-6Clo patrolling monocytes, by single cell RNA-Seq.
2019-07-31 | E-MTAB-7678 | biostudies-arrayexpress
Project description:We have previously generated ABIN1[D485N] knock-in mice that appear relatively normal for 2 months after birth, but develop large spleen at 3 months, which is followed by the appearance of high levels of antibodies against self DNA and self-nuclear antigens and severe inflammation of the kidney and other tissues after 4-5 months, hall marks of lupus like autoimmunity. Autoimmunity in ABIN1[D485N] mice appears to be caused by hyper activation of pathogen sensing Toll-like Receptor (TLR) pathway, because the phenotype of the ABIN1[D485N] mice is completely suppressed by crossing them to mice that are either lacking or expressing functionally defective proteins, which play key role in TLR signalling. MyD88 KO, IRAK4 or IRAK1 kinase-inactive knock-in mice. However, cell type(s) required to drive lupus, and how this contributes to the development of the pathology, is unknown. Recently, we have identified atypical myeloid (CD11b+ve) populations in the blood, lungs liver, kidney and spleen of ABIN1[D485N] mice. Importantly, these cells are detectable at four weeks, at least two months before auto-antibodies are detected in the serum. More detailed flow cytometry analysis of these cells revealed that, in the blood, the majority were CD115+ve and these cells could be further subdivided into Ly6C+ve and Ly6C-ve, which are characteristics of the inflammatory and patrolling monocytes, respectively. While in the lungs and spleen of WT mice the Ly6C-ve CD115+ve (patrolling monocytes) are almost absent, in the ABIN1[D485N] mice this population is more than 20-fold increased. There is also increase in the number of neutrophil population (CD11b+ GR-1hi) in the spleen of the ABIN1[D485N] mice. Although we have shown that the formation of these atypical myeloid cells proceeds the development of auto-antibodies and organ inflammation in the ABIN1[D485] mice, the signalling pathway leading to formation of these cells and their role in autoimmunity is unknown. We therefore undertook RNAseq analysis to characterise these cells in more detail. The atypical CD11b+ve cells present in spleen of ABIN1[D485N] mice are heterogeneous with three major populations, neutrophils (CD11b+ GR-1hi), Ly6C+veCD115+ve cells and Ly6C-veCD115+ve. How these cell populations in ABIN1[D485N] mice relate to one another, and whether they share a common precursor is unknown. In order to profile the cells, the neutrophils, Ly6C+veCD115+ve cells and Ly6C-veCD115+ve populations were purified by cell sorting and RNAseq analysis carried out. The RNA seq analysis was carried out with at least four replicate samples from each cell populations from ABIN1[D485N] and WT controls.
2019-11-04 | E-MTAB-8185 | biostudies-arrayexpress