Analysis of transcriptional changes induced in TSLP in CD4+ T cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA613042 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11321100_1.fastq.gz | Fastqsanger.gz | |||
| SRR11321100_2.fastq.gz | Fastqsanger.gz | |||
| SRR11321101_1.fastq.gz | Fastqsanger.gz | |||
| SRR11321101_2.fastq.gz | Fastqsanger.gz | |||
| SRR11321102_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 20 |
Similar Datasets
Project description:TSLP-stimulated CD4+ T cells block the promotion of breats tumor in mice. In this experiment, we analyze the differences in gene expression profiles of CD4+ T cells in PyMT mice in presence or absence of TSLP-stimulated CD4+ T cell
2022-05-15 | GSE147106 | GEO
Project description:Analysis of transcriptional changes induced in PyMT breast tumor by TSLP stimulated CD4+ T cells
| PRJNA612871 | ENA
Project description:TSLP-stimulated CD4+ T cells block the promotion of breats tumor in mice. In this experiment, we analyze the differences in gene expression profiles of PyMT breast tumors in presence or absence of TSLP-stimulated CD4+ T cell
2022-05-15 | GSE147067 | GEO
Project description:TSLP-stimulated CD4+ T cells block the promotion of breast cancer in a spontaneous PyMT mouse model. The goal of this project is to investigate what are the epigenetic changes induced by CD4+ T cells that lead to diminished proliferation of cancer cells
2022-05-15 | GSE156117 | GEO
Project description:Thymic stromal lymphopoietin (TSLP) is a type I cytokine that plays a central role in induction of allergic inflammatory responses. Its principal targets have been reported to be dendritic cells and / or CD4 T cells; epithelial cells are a principal source. We report here the development of a reporter mouse (TSLP-ZsG) in which a ZsGreen (ZsG)-encoding construct has been inserted by recombineering into a bacterial artificial chromosome (BAC) immediately at the translation initiating ATG of TSLP. The expression of ZsG by mice transgenic for the recombinant BAC appears to be a faithful surrogate for TSLP expression, particularly in keratinocytes and medullary thymic epithelials cells (mTECs). A comparison of gene expression in ZsG expressing and ZsG negative mTECs and cortical thymic epithelial cells, which are all ZsG negative, revealed that all three populations can be distinguished from one another. In particular ZsG (and TSLP) expressing mTECs and ZsG- mTECs are separable populations based on gene expression profiling. Little or no expression of ZsG is observed in bone marrow-derived mast cells or basophils or in CD45+ cells infiltrating TSLP/ZsG-expressing skin. Using the TSLP-ZsG reporter mouse, we show that TNFa and IL-4/IL-13 are potent inducers of TSLP expression by keratinocytes and that local activation of Th2 and Th1 cells induces keratinocyte TSLP expression. We suggest that the capacity of TSLP to both induce Th2 differentiation and to be induced by activated Th2 cells raises the possibility that TSLP may be involved in a positive feedback loop to enhance allergic inflammatory conditions.
2015-01-06 | GSE54343 | GEO
Project description:Extramedullary hematopoiesis (EMH) refers to the differentiation of hematopoietic stem cells (HSCs) into effector cells that occurs in compartments outside of the bone marrow. Previous studies linked pattern recognition receptor (PRR)-expressing HSCs, EMH and immune responses to microbial stimuli. However, the factors that regulate EMH and whether EMH operates in broader immune contexts remain unknown. Here, we demonstrate a previously unrecognized role for thymic stromal lymphopoietin (TSLP) in promoting the population expansion of progenitor cells in the periphery and identify that TSLP-elicited progenitors differentiate into effector cells including macrophages, dendritic cells and granulocytes that contribute to TH2 cytokine responses. The frequency of circulating progenitor cells was also increased in allergic patients with a gain-of-function polymorphism in TSLP, suggesting the TSLP-EMH pathway may operate in human disease. These data identify that TSLP-induced EMH contributes to the development of allergic inflammation and indicate that EMH is a conserved mechanism of innate immunity. In this study, we performed gene expression profiling to examine how the transcriptional signatures compared between TSLP-elcited GMP-like cells and naïve bone marrow-resident GMPs. Splenic TSLP-elicited GMP-like cells (CD3-, CD4-, CD5-, CD8-, CD19-, CD11b-, CD11c-, NK1.1-, FcεRI-, CD34+ c-kit+) were sort-purified from the spleen of C57BL/6 mice on day 5 post-TSLP-cDNA treatment. BM-resident GMPs (CD3-, CD4-, CD5-, CD8-, CD19-, CD11b-, CD11c-, NK1.1-, FcεRI-, Sca1- c-kit+ CD34+ CD16/32+) were sort-purified from mice that received a control-cDNA injection.
2014-03-28 | E-GEOD-52485 | biostudies-arrayexpress
Project description:Pathogenesis of allergic diseases including asthma is strongly associated with robust responses of allergen-specific Th2 cells, which produce high levels of IL-4, IL-5, IL-9, and IL-13. Despite evidence for pathogenic Th2 cells in the induction and propagation of allergic disorders, signals required for differentiation of such cells remain largely unknown. Thymic stromal lymphopoietin (TSLP) is a cytokine that is expressed upon epithelial injury, dysfunction or infection and is strongly implicated in the pathogenesis of atopic dermatitis (AD) and asthma. Although indirect regulation of Th2 differentiation via TSLP-stimulated dendritic cells well known, direct effects of TSLP on Th2 differentiation in vivo have not been rigorously analyzed. We show that TSLP may initiate Th2 response independent on IL-4 signal and increases sensitivity of CD4 cells to IL-4 stimulation inducing more robust expression of IL-4, IL-5, and IL-13 by human and mouse CD4 cells. This more potent effector state appears to be stably programmed in memory Th2 cells. As part of molecular mechanism, we demonstrate that TSLP and IL-4 signals induce distinctive genome wide alterations in activating histone modification (H3K27Ac, H3K36Me3, and H3K4Me3). We propose that TSLP acts in coordination with IL-4 to generate a more potent Th2 state that could underlie persistence and propagation of allergic disorders.
2017-04-01 | GSE81384 | GEO
Project description:The cytokine TSLP stimulates in vitro proliferation of human fetal B cell progenitors. Genetic alterations that cause overexpression of the TSLP receptor component, CRLF2, lead to B cell acute lymphoblastic leukemia (CRLF2 B-ALL) with poor outcome. The in vivo role of TSLP in normal human B cell development and its contribution to CRLF2 B-ALL are unknown. In classic xenograft models CRLF2-mediated signaling is unlikely to be activated by mouse TSLP, based on data from engineered cellular models. Here, we show that mouse TSLP does not induce activation of the CRLF-2 downstream pathways (JAK/STAT and AKT/mTOR) that are induced by human TSLP (hTSLP) in CRLF2 B-ALL cells. Based on this, we developed a novel human-mouse xenograft model system comprised of mice that produce hTSLP (+T mice) to activate human CRLF2-mediated signaling and mice that lack hTSLP (–T mice). Normal serum levels of hTSLP were achieved in +T mice, while hTSLP was undetectable in –T mice. hTSLP produced by stroma induced JAK/STAT and AKT/mTOR pathway activation and showed functional in vivo effects on normal human B cell progenitors and primary CRLF2 B-ALL cells. Whole genome microarray of primary CRLF2 B-ALL showed an induction of mTOR regulated gene expression and preservation of TSLP responsiveness in cells expanded in +T mice as compared to –T mice.
2016-05-03 | GSE65274 | GEO
Project description:The ontogeny of human Langerhans cells (LCs) remains poorly characterized, in particular the nature of LC precursors and the factors that may drive LC differentiation. Through a systematic transcriptomic analysis of TSLP-activated dendritic cells (DCs), we unexpectedly identified markers that have been associated with a skin-homing potential as well as with a LC phenotype. We performed transcriptomic analysis of TSLP-activated blood DCs, as compared to freshly purified, Medium-, and TNF-activated DCs. Among TSLP up-regulated genes, we identified molecules associated with skin homing, LC phenotype, and LC function, as determined by a literature-based survey. Conversely, genes not expressed in LCs were not found among TSLP-induced genes. Further experiments showed that TGF-? synergized with TSLP leading to the differentiation of blood BDCA-1+ DCs into bona fide Birbeck granule-positive LCs. The ontogeny of human Langerhans cells (LCs) remains poorly characterized, in particular the nature of LC precursors and the factors that may drive LC differentiation. Through a systematic transcriptomic analysis of TSLP-activated dendritic cells (DCs), we unexpectedly identified markers that have been associated with a skin-homing potential as well as with a LC phenotype. We performed transcriptomic analysis of TSLP-activated blood DCs, as compared to freshly purified, Medium-, and TNF-activated DCs. Among TSLP up-regulated genes, we identified molecules associated with skin homing, LC phenotype, and LC function, as determined by a literature-based survey. Conversely, genes not expressed in LCs were not found among TSLP-induced genes. Further experiments showed that TGF-? synergized with TSLP leading to the differentiation of blood BDCA-1+ DCs into bona fide Birbeck granule-positive LCs. Dendritic cells (DC) were purified from the blood of healthy human donors. Each replicate comes from a different donor. There are 6 freshly purified samples (Control_0h), 4 DC samples cultured during 6h with no additional stimulus than the medium (Control_6h), 5 samples cultured during 6h with recombinant TSLP (Thymic Stromal Lymphopoietin at 20 ng/uL) (TSLP_6h) and 3 samples cultured during 6h with recombinant TNF (Tumor necrosis factor at 20 ng/mL) (TNF_6h).
2014-08-01 | E-GEOD-59237 | biostudies-arrayexpress
Project description:The ontogeny of human Langerhans cells (LCs) remains poorly characterized, in particular the nature of LC precursors and the factors that may drive LC differentiation. Through a systematic transcriptomic analysis of TSLP-activated dendritic cells (DCs), we unexpectedly identified markers that have been associated with a skin-homing potential as well as with a LC phenotype. We performed transcriptomic analysis of TSLP-activated blood DCs, as compared to freshly purified, Medium-, and TNF-activated DCs. Among TSLP up-regulated genes, we identified molecules associated with skin homing, LC phenotype, and LC function, as determined by a literature-based survey. Conversely, genes not expressed in LCs were not found among TSLP-induced genes. Further experiments showed that TGF-β synergized with TSLP leading to the differentiation of blood BDCA-1+ DCs into bona fide Birbeck granule-positive LCs. The ontogeny of human Langerhans cells (LCs) remains poorly characterized, in particular the nature of LC precursors and the factors that may drive LC differentiation. Through a systematic transcriptomic analysis of TSLP-activated dendritic cells (DCs), we unexpectedly identified markers that have been associated with a skin-homing potential as well as with a LC phenotype. We performed transcriptomic analysis of TSLP-activated blood DCs, as compared to freshly purified, Medium-, and TNF-activated DCs. Among TSLP up-regulated genes, we identified molecules associated with skin homing, LC phenotype, and LC function, as determined by a literature-based survey. Conversely, genes not expressed in LCs were not found among TSLP-induced genes. Further experiments showed that TGF-β synergized with TSLP leading to the differentiation of blood BDCA-1+ DCs into bona fide Birbeck granule-positive LCs.
2014-08-01 | GSE59237 | GEO