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CCR7L-inducible lnc-Dpf3 restrains dendritic cell migration by inhibiting HIF1α-mediated glycolysis (lncRNA)

ABSTRACT: Purpose: The purpose is to systemically identify long non-coding RNAs (lncRNAs) in CCR7 Ligands-stimulated mDCs Methods: We profiled lncRNA seq in mDCs stimulated with or without CCR7 ligand CCL19 and CCL21. Results: CCR7 stimulation induced profound lncRNAs expression in mDCs

ORGANISM(S): Mus musculus

PROVIDER: GSE118533 | GEO | 2020/05/25

REPOSITORIES: GEO

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CCR7L-inducible lnc-Dpf3 restrains dendritic cell migration by inhibiting HIF1α-mediated glycolysis (mRNA)

Project description:Purpose: The purpose is to systemically identify RNA expression changes after lnc-Dpf3 knockdown in CCR7-stimulated mDCs Methods: We profiled RNA seq in mDCs transfected with si-Lnc-Dpf3 or si-NC and stimulated with or without CCR7 ligand CCL19 and CCL21. Results: CCR7 stimulation induced profound RNA expression changes in mDCs, and a set of genes were differentially expressed in lnc-Dpf3-knockdown DC

2020-05-25 | GSE118531 | GEO

Glycosyltransferase Extl1 promotes CCR7-mediated dendritic cell migration to restrain infection and autoimmunity [treated vs. untreated]

Project description:Purpose: mRNAs sequencing of the gene expression differences in CCR7-stimulated mDC. The goals of this study are to investigate the biological effect of glycosyltransferase Extl1 in regulating dendritic cell function.

2023-01-19 | GSE184858 | GEO

Homo sapiens

Project description:BDCA1+ mDCs and BDCA3+ mDCs stimulated with vaccines for 6 hr

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Genome wide mapping of long noncoding (lnc) RNAs in hepatic stellate cells

Project description:Hepatic stellate cells are the primary cell type responsible for development of fibrosis in chronic liver disease. We used directional RNA sequencing (RNA-seq) and chromatin immunoprecipitation and sequencing (ChIP-seq) to identify the lncRNAs expressed in human HSCs. We also identified the lncRNAs that change in expression with differentiation of nonfibrotic quiescent HSCs into fibrotic HSC myofibroblasts and those that are regulated by TGF-beta signaling. ChIP-seq was also performed to identify DNA regions occupied by H3K27ac to define super-enhancers in HSC myofibroblasts. This study identified lncRNAs expressed HSCs that may regulate fibrosis. Analysis of genome-wide lncRNA expression using RNA-seq and ChiP-seq in human HSCs under four different conditions

2016-03-23 | E-GEOD-68108 | biostudies-arrayexpress

GATA1-deficient dendritic cells display impaired CCL21-dependent migration towards lymph nodes due to reduced levels of polysialic acid

Project description:Dendritic cells (DCs) play a pivotal role in the regulation of the immune response. DC development and activation is finely orchestrated through transcriptional programs. GATA1 transcription factor is required for murine DC development and data suggests that it might be involved in the fine-tuning of the life span and function of activated DCs. We generated DC-specific Gata1 knockout mice (Gata1-KODC), which presented a 20% reduction of splenic DCs, partially explained by enhanced apoptosis. RNA-Seq analysis revealed a number of deregulated genes involved in cell survival, migration and function. DC migration towards peripheral lymph nodes was impaired in Gata1-KODC mice. Migration assays performed in vitro showed that this defect was selective for CCL21, but not CCL19. Interestingly, we show that Gata1-KODC DCs have reduced polysialic acid levels on their surface, which is a known determinant for the proper migration of DCs towards CCL21.

2016-11-08 | GSE69969 | GEO

Transcriptional profiling of ex vivo isolated inflammed mouse lymphatic endothelial cells

Project description:Chemokines and adhesion molecules upregulated in lymphatic endothelial cells (LECs) during tissue inflammation are believed to enhance dendritic cell (DC) migration to draining lymph nodes (dLNs), but the in vivo control of this process is not well understood. By performing transcriptional profiling of LECs isolated from murine skin, we found that inflammation induced by a contact hypersensitivity (CHS) response upregulated the adhesion molecules ICAM-1 and VCAM-1 and inflammatory chemokines in LECs. Furthermore, lymphatic lineage markers like Prox-1, VEGFR3 and LYVE-1 were significantly downregulated during CHS. By contrast, skin inflammation induced by Complete FreundM-bM-^@M-^Ys adjuvant (CFA) induced a different pattern of chemokine and lymphatic marker gene expression and almost no ICAM-1 up-regulation in LECs. In FITC painting experiments, DC migration to dLNs was more strongly increased in CFA- as compared to CHS-induced inflammation. Interestingly, DC migration did not correlate with the induction of CCL21 and ICAM-1 in LECs. However, the requirement for CCR7 signaling became further pronounced during inflammation, whereas CCR7-independent signals only had a minor role in enhancing DC migration. Collectively, these findings indicate that inflammation-induced DC migration is stimulus-dependent and only moderately enhanced by LEC-induced genes other than CCL21. Mouse ear skin single-cell suspensions were prepared by a fast protocol that minimizes the RNA degradation. Fluorescence-activated cell sorting (FACS) was used to sort lymphatic endothelial cells (LEC) from CHS inflammed and control skin. 4 pairs (each with one control and one CHS inflammed sample, sorted and extracted on the same day) of LECs were chosen based on the quality of extracted and amplified material. This gave 8 samples to analyze (4 biological replicates in each condition). Each sample was sorted from 3 mice.

2011-05-19 | E-GEOD-26229 | biostudies-arrayexpress

Transcriptional profiling of ex vivo isolated inflammed mouse lymphatic endothelial cells

Project description:Chemokines and adhesion molecules upregulated in lymphatic endothelial cells (LECs) during tissue inflammation are believed to enhance dendritic cell (DC) migration to draining lymph nodes (dLNs), but the in vivo control of this process is not well understood. By performing transcriptional profiling of LECs isolated from murine skin, we found that inflammation induced by a contact hypersensitivity (CHS) response upregulated the adhesion molecules ICAM-1 and VCAM-1 and inflammatory chemokines in LECs. Furthermore, lymphatic lineage markers like Prox-1, VEGFR3 and LYVE-1 were significantly downregulated during CHS. By contrast, skin inflammation induced by Complete Freund’s adjuvant (CFA) induced a different pattern of chemokine and lymphatic marker gene expression and almost no ICAM-1 up-regulation in LECs. In FITC painting experiments, DC migration to dLNs was more strongly increased in CFA- as compared to CHS-induced inflammation. Interestingly, DC migration did not correlate with the induction of CCL21 and ICAM-1 in LECs. However, the requirement for CCR7 signaling became further pronounced during inflammation, whereas CCR7-independent signals only had a minor role in enhancing DC migration. Collectively, these findings indicate that inflammation-induced DC migration is stimulus-dependent and only moderately enhanced by LEC-induced genes other than CCL21.

2011-05-20 | GSE26229 | GEO

CCR7L-inducible lnc-Dpf3 restrains dendritic cell migration by inhibiting HIF1α-mediated glycolysis (mRNA)

Project description:CCR7L-inducible lnc-Dpf3 restrains dendritic cell migration by inhibiting HIF1α-mediated glycolysis (mRNA)

| PRJNA485962 | ENA

CCR7L-inducible lnc-Dpf3 restrains dendritic cell migration by inhibiting HIF1α-mediated glycolysis (lncRNA)

Project description:CCR7L-inducible lnc-Dpf3 restrains dendritic cell migration by inhibiting HIF1α-mediated glycolysis (lncRNA)

| PRJNA485961 | ENA

Transcription profiling of human T cells to determine the strength of T cell stimulation

Project description:The strength of T cell stimulation determines IL-7 responsiveness, recall potential and lineage commitment of primed human CD4+IL-7Rhi T cells; We analyzed how the strength of antigenic stimulation - as determined by dendritic cell (DC) number, DC maturation state and antigen concentration - controls in human CD4+ T cells IL-7R? expression and responsiveness to IL-7, IL-15 and antigen. We found that T cells primed by different strengths of stimulation expressed IL-7R? in different proportions and preferentially on cells that maintained expression of the central memory marker CCR7. However, while CCR7+IL-7Rhi cells generated at high strength of stimulation proliferated vigorously in response to IL-7 or IL-15, CCR7+IL-7Rhi cells generated at low strength of stimulation responded poorly. High cytokine responsiveness was associated with reduced PTEN expression and enhanced s6-kinase activation, consistent with efficient receptor coupling to downstream signalling pathways. Interestingly, while intermediate-stimulated CCR7+IL-7Rhi cells were non-polarized, self-renewed with IL-7 and expanded with antigen, high-stimulated cells generated Th1 effector cells with cytokines but showed impaired IL-2 production and survival with antigen. Gene expression analysis suggested that high-stimulated cells represented pre-Th1 cells with low recall potential and high metabolic state. Taken together these results demonstrate that IL-7 receptor expression and coupling are instructed in T cells by the strength of stimulation and suggest that memory subsets may derive from CCR7+IL-7Rhi precursors that received different strengths of stimulation. Experiment Overall Design: two samples treated with weaker dendritic stimulus, two samples treated with stonger dendritic stimulus.

2008-06-14 | E-GEOD-6566 | biostudies-arrayexpress

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