Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA197287 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Activating CD8 T cell clones via the T cell receptor complex in the absence and presence of cyclosporine A
2015-07-13 | E-GEOD-46122 | ExpressionAtlas
Project description:Comparison of a cyclosporine-resistant murine CD8 T cell clone to a cyclosporine-sensitive murine T cell clone during activation (CSA = Cyclosporine A) Chronic allograft rejection is the leading cause of morbidity/mortality in solid organ and bone marrow transplant patients. It occurs in the setting of potent calcineurin and mTOR inhibitor therapies, implying that T cells mediating chronic rejection can function with compromised calcineurin-NFAT or IL-2 receptor signaling pathways. In murine models the T cells mediating allograft rejection in the setting of calcineurin inhibitor therapy are CD8 T cells making IFN-gamma without a requirement for perforin. It is not known whether these pathologic T cells are a unique subset or how they function. In parallel other animal model research has shown that alloepthelial cells residing in the donor organ are critical targets for rejection. While investigating T cell-alloepithelial cell interactions, we discovered an unusual alloreactive CD8 T cell population that recognized MHC class II I-Abm12. A CD8 T cell clone derived from that population was intrinsically-resistant to cyclosporine and rapamycin without prior exposure to either in vivo or in vitro. Microarray analysis comparing the novel CD8 T cell clone to a conventional CD8 CTL clone specific for MHC class I Kbm1 suggested that the TCR signaling pathway responsible for cyclosporine-resistance utilized the Aryl Hydrocarbon Receptor (AHR). Two T cell clones x 2 experimental conditions x 4 replicates
2014-04-14 | E-GEOD-46122 | biostudies-arrayexpress
Project description:Comparison of a cyclosporine-resistant murine CD8 T cell clone to a cyclosporine-sensitive murine T cell clone during activation (CSA = Cyclosporine A) Chronic allograft rejection is the leading cause of morbidity/mortality in solid organ and bone marrow transplant patients. It occurs in the setting of potent calcineurin and mTOR inhibitor therapies, implying that T cells mediating chronic rejection can function with compromised calcineurin-NFAT or IL-2 receptor signaling pathways. In murine models the T cells mediating allograft rejection in the setting of calcineurin inhibitor therapy are CD8 T cells making IFN-gamma without a requirement for perforin. It is not known whether these pathologic T cells are a unique subset or how they function. In parallel other animal model research has shown that alloepthelial cells residing in the donor organ are critical targets for rejection. While investigating T cell-alloepithelial cell interactions, we discovered an unusual alloreactive CD8 T cell population that recognized MHC class II I-Abm12. A CD8 T cell clone derived from that population was intrinsically-resistant to cyclosporine and rapamycin without prior exposure to either in vivo or in vitro. Microarray analysis comparing the novel CD8 T cell clone to a conventional CD8 CTL clone specific for MHC class I Kbm1 suggested that the TCR signaling pathway responsible for cyclosporine-resistance utilized the Aryl Hydrocarbon Receptor (AHR).
2014-04-14 | GSE46122 | GEO
Project description:To investigate type I interferon regulated genes in CD8+ T cells, we used microarray analyses after stimulation of primary murine T cell cultures. Negatively sorted T cells from naive C57Bl/6 mice were incubated with PBS or anti-CD3 in presence or absence of type I interferon (IFN-4a, 500U/mL). After 6h total RNA was extracted from the primary T cell cultures and microarrays were performed after RNA quality control. Among significantly regulated genes, we identified NK cell receptor ligands to be affected by exposure to type I interferon. 10^6 negatively sorted CD8+ T cells were stimulated with anti-CD3 antibody in the presence or absence of IFN-4a. Additionally, CD8+ cells were mock treated with PBS in the presence or absence of IFN-4a. After 6h, total RNA was extracted from cell suspensions and microarray analyses were performed. All experiments were carried out in triplicates.
2014-06-30 | E-GEOD-57421 | biostudies-arrayexpress
Project description:Human low passage melanoma cell lines were compared after 24h culture alone or in presence of melanoma-specific CD8+ T cell clones
2016-08-30 | GSE79991 | GEO
Project description:We report the gene expression differences between OT-1 T cells activated alone or in the presence of TLR1/2 (Pam3CSK4) or TLR7 (Gardiquimod). By activating OT-1 splenocytes in the presence or absence of the TLR agonists, isolating RNA from purified CD8+ T cells we show that cells activated in the presence of either TLR1/2 or TLR7 agonists had similar transcriptional profiles demonstrating an increase in Th1 cytokine expression over cells that were activated alone. This study provides a key piece of information for those designing T cell mediated therapies.
2018-12-26 | GSE110144 | GEO
Project description:The aim of this work was to identify functional features that are specific of human Treg cells, through the identification of genes that are differentially expressed: 1/ in activated Treg clones versus activated Thelper clones; 2/ in Th clones activated in the presence versus the absence of TGFb; 3/ in suppressed Th clones, i.e. Th clones activated in the presence of Treg clones, versus controls. Keywords: TCR activation
2009-01-09 | GSE14330 | GEO
Project description:CD8+ T cells derived from mice with intact NLRP3 signaling in the tumor microenvironment showed an increased expression of coinhibitory receptors PD-1, TIM-3, 2B4 and LAG-3 compared to CD8+ T cells from PancOVA-bearing Nlrp3-/- mice, indicating that NLRP3 inflammasome activation in the tumor microenvironment mediates IL-18 receptor signaling-induced T cell exhaustion. RNAseq was used to characterised molecular pathways involved in T cell plasticity in the presence and absence of intratumoral NLRP3.
2022-04-14 | GSE200570 | GEO
Project description:TC-510 is a novel cell therapy that consists of autologous genetically engineered T cells expressing two synthetic constructs: first, a single-domain antibody that recognizes human Mesothelin, fused to the CD3-epsilon subunit which, upon expression, is incorporated into the endogenous T cell receptor (TCR) complex and second, a PD-1:CD28 switch receptor, which is expressed on the surface of the T cell, independently from the TCR. The PD-1:CD28 switch receptor comprises the PD-1 extracellular domain fused to the CD28 intracellular domain via a transmembrane domain. Thus, the switch is designed to produce a costimulatory signal upon engagement with PD-L1 on cancer cells.
| 2740481 | ecrin-mdr-crc
Project description:Background and methods: Ruxolitinib (RUX), a Jak1/2 inhibitor, has been reported to attenuate murine bone marrow failure recently. Its potential toxocicty of anemia and thrombocytopenia in human remains a concern. To minimize its potential toxoxicity, we tested therapeutic effectsof low dose ruxolitinib plus cyclosporine in murine model of immune-mediated bone marrow failure. Bone marrow CD8 and CD4 T cells were sorted from treated or untreated bone marrow failure mice. RNA-Seq and analysis was performed using SMART-Seq mRNA LP Kit (Takara) and the Illumina Novaseq6000, according to the Institute's protocols. Results: low dose of ruxolitinib plus cyclosporine improved pancytopenia and BM cellularity and decreased BM T cell infiltration in bone marrow failure mice. RNA sequencing demonstrated that low dose of ruxolitinib plus cyclosporine suppressed immune-related pathways in bone marrow infiltrated CD8 T cells and MHC-II expression in CD4 T cells compared with untreated mice. Conclusion: Our results demonstrate that low dose of ruxolitinib plus cyclosporine remains the efficacy in attenuation of disease and extending survival of immune-mediated bone marrow failure mice.
2024-05-08 | GSE240864 | GEO