RNA-sequencing analysis of regulatory T cells differentiated in presence or absence of CPI-1205
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE114717 | GEO | 2018/05/22
REPOSITORIES: GEO
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Project description:RNA-sequencing analysis of regulatory T cells differentiated in presence or absence of CPI-1205
| PRJNA472362 | ENA
Project description:Background: Ascaris lumbricoides cystatin (Al-CPI) prevents development of allergic airway inflammation and colitis in mice models. It has been suggested that helminth derived cystatins inhibit cathepsins in dendritic cells (DC), but their immunomodulatory mechanisms are unclear. We aimed to analyze the transcriptional profile of human monocyte derived DC (moDC) upon stimulation with Al-CPI to elucidate target genes and pathways of parasite immunomodulation. Methods: moDC were generated from peripheral blood monocytes from six healthy human donors of Denmark, stimulated with 1 μM of Al-CPI and cultured for 5 hours at 37°C. RNA was sequenced using TrueSeq RNA libraries and the NextSeq 550 v2.5 (75 cycles) sequencing kit (Illumina, Inc). After QC, reads were aligned to the human GRCh38 genome using STAR. Differential expression was calculated by DESEq2 and expressed in fold changes (FC). Cell surface markers and cytokine production by moDC were evaluated by flow cytometry. Results: Compared to unstimulated cells, Al‐CPI stimulated moDC showed differential expression of 444 transcripts (|FC| ≥1.3). The top significant differences were in kruppel like factor 10 (KLF10, FC 3.3, PBH = 3 x 10-136 ), palladin (FC 2, PBH = 3 x 10-41 ) and the low-density lipoprotein receptor (LDLR, FC 2.6, PBH = 5 x 10-41 ). Upregulated genes were enriched in regulation of cholesterol biosynthesis by sterol regulatory element-binding proteins (SREBP) signaling pathways. Several genes in the cholesterol biosynthetic pathway showed significantly increased expression upon Al-CPI stimulation, even in the presence of LPS. Regarding the pathway of negative regulation of immune response, we found significant decrease in cell surface expression of CD86, HLA-DR and PD-L1 upon stimulation with 1 μM Al-CPI. Conclusion: Al-CPI modifies the transcriptome of moDC, increasing several transcripts encoding enzymes involved in cholesterol biosynthesis and SREBP signaling. Moreover, Al-CPI target several transcripts in the TNF-alpha signaling pathway influencing cytokine release by moDC. Several SMADs, members of the TGF-beta and the IL-10 families, including KLF10 were also This is a provisional file, not the final typeset article modified by Al-CPI stimulation. The regulation of the mevalonate pathway and cholesterol biosynthesis suggests new mechanisms involved in DC responses to helminth immunomodulatory molecules.
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Project description:RNA- and ATAC-seq data from hESCs differentiated with Wnt and Activin with or without CPI-203
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Project description:These studies profiled the transcriptional differences in a human regulatory T cell-like cell line, MT-2, when FOXP3 a master transcriptional regulatory element was present or absence. In the FOXP3 null MT-2 cell line FOXP3 express had been deleted by CRISPR-Cas9. RNA was prepared for bulk RNA-seq from 4 replicates for each cell line. In the absence of FOXP3 in the MT-2 cell line there were 1251 differential expressed genes. These differentially expressed gene results indicate that hte loss of FOXP3 in MT-2 cells results in altered transcripts and pathways often associated with regultory T cell activity or phenotypes.
2023-09-21 | GSE220629 | GEO
Project description:To determine if there are differences in the gene expression profile of peripheral blood mononuclear cells in patients with Acute Myeloid Leukemia (AML) or Myelodysplastic Syndrome (MDS) who responded to CPI-613 when compared to those patients who did not respond we generated gene expression profiles from four responding patients and compared them to four non-responders. None of the gene expression profiles have been previously published. Here we describe the origins and provide associated clinical annotations with the hope that other investigators will be able to utilize this data in their own research. Peripheral blood mononuclear cells were isolated from 4 patients (3 MDS, 1 AML) who responded to treatment with CPI-613 and four patients (all with AML) who did not respond. Total RNA was isolated and gene expression levels were profiled on the Affymetrix Gene Atlas U219 array strips.
2014-08-13 | E-GEOD-60350 | biostudies-arrayexpress
Project description:These studies profiled the expression of mRNA in lung type II alveolar epithelial cells during lipopolysacchride induced lung injury in the presence or absence of Foxp3+ Regulatory T Cells Baseline, uninjured lung type II alveolar epithelial (AT2) cells or resolving AT2 cells, in the presence or absence of Foxp3+ regulatory T cells (Tregs), were sorted (7 days after intratracheal instillation of LPS for resolving conditions) and mRNAs differentially expressed (DE) between control AT2 cells, resolving AT2 cells with Tregs present, or resolving AT2 cells in mice depleted of Tregs were identified using microarrays.
2020-06-04 | GSE106081 | GEO
Project description:Transcriptional profilling of human GSC comparing undifferentiated (ND) and differentiated (Diff 0.5%) GSC treated or not with TWS119 (LW) an inhibitor of GSK3beta Glioblastomas (GBM) are the most common form of primary brain tumors. Highly vascularized, infiltrating, resistant to current therapies, they affect patients at different ages. The median survival is shorter than 18 months. GBM follow the cancer stem cell (CSC) model. This concept proposes that a minority of cells within the tumor mass, with long term self-renewal and differentiation properties, is responsible for the initiation and the growth of tumors. CSCs provide all the subtypes of cells that compose the tumor, including endothelial cells and pericytes. Their functional properties are associated with a molecular signature combining makers of neural and/or embryonic stem cells, and markers of mesenchymal cells. A growing body of evidences supports that tumorâs behavior, including proliferation, progression, invasion and â most importantly - a great part of resistance to therapies are determined by these self-renewing tumor cells. It is becoming therefore evident that failure of current treatments to eliminate glioma-initiating cells (GiCs) contributes to tumor recurrence. Targeting GiCs and their stem-like properties constitutes thus one of the main therapeutic challenges to significantly improve anti-cancer treatments. A relevant solution to target GiCs, is to force them to acquire a non self-renewing state. Under this non stem-like state, the cells lose their tumorigenicity and become vulnerable to therapies. We observed that GiC differentiation is associated to an increase of active GSK3beta expression. Suppression of this activation using a chemical inhibitor (TWS119) altered the differentiation process. To identify transcroptomic changes due to GSK3beta inhibition during differentiation, we have differentiated two GiC cultures (TG1, and TG6) treated or not with TWS119. Total mRNA have been extracted and compared to mRNA extracted from self-renewing TG1 and TG6 cells. For these experiments we used âAgilent human genome whole 44Kâ chips. two-condition experiment, undifferentiated GSC (ND) vs. Differentiated (diff 0.5%) and undifferentiated GSC (ND) versus differentiated GSC treated with TWS119 (diff 0.5%LW) in monoplicate in TG1 and in TG6 cells (two different primary cultures of GSC).
2016-03-23 | E-GEOD-79478 | biostudies-arrayexpress
Project description:Transcriptional profilling of human GSC comparing undifferentiated (ND) and differentiated (Diff 0.5%) GSC treated or not with TWS119 (LW) an inhibitor of GSK3beta Glioblastomas (GBM) are the most common form of primary brain tumors. Highly vascularized, infiltrating, resistant to current therapies, they affect patients at different ages. The median survival is shorter than 18 months. GBM follow the cancer stem cell (CSC) model. This concept proposes that a minority of cells within the tumor mass, with long term self-renewal and differentiation properties, is responsible for the initiation and the growth of tumors. CSCs provide all the subtypes of cells that compose the tumor, including endothelial cells and pericytes. Their functional properties are associated with a molecular signature combining makers of neural and/or embryonic stem cells, and markers of mesenchymal cells. A growing body of evidences supports that tumor’s behavior, including proliferation, progression, invasion and – most importantly - a great part of resistance to therapies are determined by these self-renewing tumor cells. It is becoming therefore evident that failure of current treatments to eliminate glioma-initiating cells (GiCs) contributes to tumor recurrence. Targeting GiCs and their stem-like properties constitutes thus one of the main therapeutic challenges to significantly improve anti-cancer treatments. A relevant solution to target GiCs, is to force them to acquire a non self-renewing state. Under this non stem-like state, the cells lose their tumorigenicity and become vulnerable to therapies. We observed that GiC differentiation is associated to an increase of active GSK3beta expression. Suppression of this activation using a chemical inhibitor (TWS119) altered the differentiation process. To identify transcroptomic changes due to GSK3beta inhibition during differentiation, we have differentiated two GiC cultures (TG1, and TG6) treated or not with TWS119. Total mRNA have been extracted and compared to mRNA extracted from self-renewing TG1 and TG6 cells. For these experiments we used “Agilent human genome whole 44K” chips.
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Project description:A comparative analysis of gene expression of injured skeletal muscle from wild-type (Foxp3-DTR-) and Treg-depleted (Foxp3-DTR+) mice showed that Treg cells are critical for effective repair and regeneration of acute injury of skeletal muscle.
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Project description:A comparative analysis of gene expression of injured skeletal muscle from wild-type (Foxp3-DTR-) and Treg-depleted (Foxp3-DTR+) mice showed that Treg cells are critical for effective repair and regeneration of acute injury of skeletal muscle. Foxp3-DTR+ and Foxp3-DTR- mice were injured with cardiotoxin in TA muscle at day 0 and treated with diphtheria toxin every other day from day 0 until dissection on day 4 or 8. TA muscle was flash-frozen and RNA was extracted using Trizol. RNA from whole tissue samples was amplified, labeled, and hybridized to Affymetrix Mouse Gene 1.0 ST Arrays.
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