K.Woollard_Aglient
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Nicolas Cagnard
PROVIDER: E-MEXP-3377 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Macrophages and dendritic cells (DC) are key components of cellular immunity and, as per the current model, originate from hemopoietic stem cells (HSCs). However, microglia were recently shown to originate from precursors that precede the appearance of HSCs. We thus re-investigated macrophage development and their relationship to HSCs and yolk sac (YS) precursors.
2012-03-15 | E-MEXP-3510 | biostudies-arrayexpress
Project description:To evaluate geneexpression profile in developing joints vs adjacent growth plate in control and TGF-beta type II receptor conditional knock-out in limb mesenchyjme We obtained E14.5 autopods from two normal controls and two Tgfbr2Prx1KO littermate embryos. Samples were frozen in OTC and cryosectioned and subjected to laser-capture microdissection for RNA sampling for interzone, growth plate chondrocytes and interdigital tissue. RNas were subjected to microarray analysis
2012-06-17 | E-GEOD-37287 | biostudies-arrayexpress
Project description:Purified CD4 T cells isolated from the cord blood were divided in subsets according to IL2R, IL7R and chemokine receptors (CCR6, CXCR3 and CCR4) and compared by whole genome microarray analysis. CD4 T cell memory subsets and Naive T cell collected from 3 donors (#480, #487, #488)
2014-06-04 | E-GEOD-51133 | biostudies-arrayexpress
Project description:Transcriptional profiling of subventricular zone (SVZ) progenitors comparing control healthy mice to mice induced to develop an autoimmune demyelination (EAE model). Goal was to unveil genes involved in demyelination-induced reactivity of SVZ progenitors. Two-condition experiment, healthy vs. EAE derived SVZ progenitors. Biological replicates: 2 control replicates, 2 EAE replicates. SVZ progenitors were sorted in two cell populations: neuronal progenitors (PSA-NCAM magnetic sorting) and glial progenitors (NG2 magnetic sorting). Progenitors from healthy mice are reference samples.
2013-09-09 | E-GEOD-47486 | biostudies-arrayexpress
Project description:Transcriptional profiling to examine differences resulting from priming of virus-specific CD8 T cells in draining lymph node and in bone marrow, following intradermal injection of modified virus Ankara (MVA)-HIV gag. Transcriptional profiling of mouse pentamer H2kD-AMQMLKETI (HIV-gagP24) CD8 T cells from draining lymph nodes(LN) and bone marrow (BM ) 5 days following intradermal injection of MVA-HIV gag, and compared to naive (CD62L Hi CD44 int) CD8+ T cells from lymph node of naive mice (NTc). Three-condition experiment, BM, LN and NTc. Experimental replicates: 5 BM, 5 LN, 5 NTc, RNA pooled from 3 independant experiments of 5 mice each.
2012-10-23 | E-GEOD-41736 | biostudies-arrayexpress
Project description:Background: A specific subset of regulatory IL-10 producing B cells has been extensively studied in autoimmune and inflammatory pathologies. These cells are able to constrain exacerbated inflammation by inhibiting T cell mediated responses and maturation of antigen presenting cells. In allergic diseases, observations that increase of regulatory B cells is necessary for allergen tolerance suggest that development of allergic asthma would be associated with a defect in the regulatory B cells compartment. Objective: We sought to (i) characterize regulatory IL-10+ regulatory B cell subset in Balb/c mice by microarray and flow cytometry and (ii) investigate their regulatory capacity in vivo in a house dust mite model of allergic asthma. Results: We identified an IL-10 producing B cells subset able to control T cell proliferation in vitro in both control and asthmatic mice. This subset is decreased in allergic mice. IL-10+ Breg cells express high levels of CD9 and upregulate CD70 and CD73 after activation. Expression of CD9 allows identifying more than 50% of Bregs. Interestingly CD9+ B cells inhibit TH2-TH17 allergic airway inflammation in vivo after adoptive transfer in an IL-10 dependent manner. Conclusions: Herein, we demonstrate that induction of allergic asthma dampens the generation of Bregs contributing to exacerbated airway inflammation. We identified a distinct CD9+ Breg-cell population decreased in lung of HDM mice and able to control asthma and allergic airway inflammation by producing IL-10 after adoptive transfer. This study points B cells as an interesting therapeutic target in allergic asthma. IL-10+ B cells (n=3) and 3 IL-10- B cells (n=3) in control mice + IL-10+ B cells (n=3) and 3 IL-10- B cells (n=3) from asthmatic allergic (HDM) mice
2015-03-01 | E-GEOD-57772 | biostudies-arrayexpress
Project description:The fusion of bone marrow (BM) hematopoietic cells with hepatocytes to generate BM derived hepatocytes (BMDH) is a natural process, which is enhanced in damaged tissues. However, the reprogramming needed to generate BMDH and the identity of the resultant cells are essentially unknown. In a mouse model of chronic liver damage, here we identify a modification in the chromatin structure of the hematopoietic nucleus during BMDH formation, accompanied by the sequential loss of the key hematopoietic transcription factor PU.1/Sfpi1 (SFFV proviral integration 1) and gain of the key hepatic transcriptional regulator HNF-1A homeobox A (HNF-1A/Hnf1a). Through genome-wide expression analysis of laser captured BMDH, a differential gene expression pattern was detected and the chromatin changes observed were confirmed at the chromatin regulator gene level. Similarly, Tranforming Growth Factor-M-NM-21 (TGF-M-NM-21) and neurotransmitter (e.g. Prostaglandin E Receptor 4 [Ptger4]) pathway genes were over-expressed. In summary, in vivo BMDH generation is a sequential process in which the hematopoietic cell nucleus changes its identity and acquires hepatic features. These BMDHs have their own cell identity characterized by an expression pattern different from hematopoietic cells or hepatocytes. The role of these BMDHs in the liver requires further investigation. C57BL/6JxDBA/2 F1 female mice were subjected to lethal irradiation and intravenously injected with bone marrow cells harvested from C57BL/6J-M-NM-2actinEGFPxDBA/2 F1 male mice. The livers of female mice were injured with CCl4. Liver individual cells were laser captured from frozen sections. Bone marrow derived hepatocytes (BMDH), hematopoietic cells, and hepatocytes, were analyzed individually.
2012-03-31 | E-GEOD-29878 | biostudies-arrayexpress
Project description:Long-term consumption of fatty foods is associated with obesity, macrophage activation and inflammation, metabolic imbalance, and a reduced lifespan. We took advantage of Drosophila genetics to investigate the role of macrophages and the pathway(s) that govern their response to dietary stress. Flies fed a lipid-rich diet presented with increased fat storage, systemic JAK-STAT activation, reduced insulin sensitivity and hyperglycaemia, and a shorter lifespan. Drosophila macrophages scavenged lipids and produced the type 1 cytokine upd3, in a scavenger-receptor (croquemort) and JNK-dependent manner. Genetic depletion of macrophages, or macrophage-specific silencing of upd3 decreased JAK-STAT activation and rescued insulin sensitivity and the lifespan of Drosophila, but did not decrease fat storage. NF-M-NM-:B signalling made no contribution to the phenotype observed. These results identify an evolutionarily conserved M-bM-^@M-^Xscavenger receptor-JNK-Type 1 cytokineM-bM-^@M-^Y cassette in macrophages, which controls glucose metabolism and reduces lifespan in Drosophila maintained on a lipid-rich diet via activation of the JAK-STAT pathway Long-term consumption of fatty foods is associated with obesity, macrophage activation and inflammation, metabolic imbalance, and a reduced lifespan. We took advantage of Drosophila genetics to investigate the role of macrophages and the pathway(s) that govern their response to dietary stress. Flies fed a lipid-rich diet presented with increased fat storage, systemic JAK-STAT activation, reduced insulin sensitivity and hyperglycaemia, and a shorter lifespan. Drosophila macrophages scavenged lipids and produced the type 1 cytokine upd3, in a scavenger-receptor (croquemort) and JNK-dependent manner. Genetic depletion of macrophages, or macrophage-specific silencing of upd3 decreased JAK-STAT activation and rescued insulin sensitivity and the lifespan of Drosophila, but did not decrease fat storage. NF-M-NM-:B signalling made no contribution to the phenotype observed. These results identify an evolutionarily conserved M-bM-^@M-^Xscavenger receptor-JNK-Type 1 cytokineM-bM-^@M-^Y cassette in macrophages, which controls glucose metabolism and reduces lifespan in Drosophila maintained on a lipid-rich diet via activation of the JAK-STAT pathway 5 biological samples were FACS-sorted from different batches of Drosophila melanogaster males after 30 days on 15% lipid enriched diet (n=5) and control diet (n=5)
2015-01-30 | E-GEOD-63254 | biostudies-arrayexpress
Project description:Considerable information has accumulated about components of bone marrow that regulate survival, self-renewal and differentiation of hematopoietic cells. We have now studied Wnt signaling in that context, assessing influences on human and murine hematopoiesis. Microarray, PCR and staining experiments revealed that OP9 acquired osteoblastic characteristics while down-regulating some features associated with mesenchymal stem cells. This included down-regulation of Angiopoietin 1, c-Kit ligand and VCAM-1 expression. In contrast, production of decorin, tenascins and fibromodulin markedly increased. At least one of these extracellular matrix components, decorin is a regulator of hematopoiesis. That is, addition of the protein to OP9 co-cultures causes changes similar to Wnt3a. Two control samples (LZR1 & LZR2) were analyzed from OP9 mouse stromal cells transfected with vector only, and two experimental samples (W3A1 & W3A2) were analyzed from OP9 cells transfected with vector containing the Wnt3A gene.
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