Gene expression profile of SmarT-cells compared to control 1G CAR T cells
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PROVIDER: PRJNA451006 | ENA |
REPOSITORIES: ENA
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Project description:The objective of this experiment was to compare the transcriptional profile of T cells modified to express CAR, TBBR and 4/7 ICR (i.e. SmarT-cells) against control 1G CAR T cells expressing CD3z endodomain. RNA samples were isolated from trangenic T cells generated from three independent donors.
2018-04-20 | GSE113391 | GEO
Project description:The objective of this experiment was to compare the transcriptional profile of T cells modified to express CAR, TBBR and 4/7 ICR (i.e. SmarT-cells) against control T cells expressing the delta constructs (i.e. ΔCAR, ΔTGFbRII and ΔIL4R). RNA samples were isolated from trangenic T cells generated from three independent donors.
2018-04-20 | GSE113390 | GEO
Project description:This study tested the hypothesis that transcription of immediate early genes is inhibited in T cells activated in microgravity (mg). Immunosuppression during spaceflight is a major barrier to safe long-term human space habitation and travel. The goals of these experiments were to prove that mg was the cause of impaired T cell activation during spaceflight as well as understand the mechanisms controlling early T cell activation. T cells from 4 human donors were stimulated with concanavalin A (ConA) and anti-CD28 onboard the International Space Station (ISS). An onboard centrifuge was used to generate a 1g simultaneous control to isolate the effects of mg from other variables of spaceflight. Microarray expression analysis after 1.5 hours of activation demonstrated that mg- and 1g-activated T cells had distinct patterns of global gene expression and identified 47 genes that were significantly differentially down-regulated in mg. Importantly, several key immediate early genes were inhibited in mg.
2012-06-21 | GSE38836 | GEO
Project description:This study tested the hypothesis that transcription of immediate early genes is inhibited in T cells activated in microgravity (mg). Immunosuppression during spaceflight is a major barrier to safe long-term human space habitation and travel. The goals of these experiments were to prove that mg was the cause of impaired T cell activation during spaceflight as well as understand the mechanisms controlling early T cell activation. T cells from 4 human donors were stimulated with concanavalin A (ConA) and anti-CD28 onboard the International Space Station (ISS). An onboard centrifuge was used to generate a 1g simultaneous control to isolate the effects of mg from other variables of spaceflight. Microarray expression analysis after 1.5 hours of activation demonstrated that mg- and 1g-activated T cells had distinct patterns of global gene expression and identified 47 genes that were significantly differentially down-regulated in mg. Importantly, several key immediate early genes were inhibited in mg. T cells were isolated from human volunteers. T cells from each donor were kept separate and loaded into individual chambers in separate cassettes for the following treatments: mg non-activated, mg activated, and 1g activated. Therefore, samples represent biological triplicates. Experimental units were launched into space and placed into the KUBIK facility onboard the International Space Station. The 1g units were placed in the central centrifuge positions and centrifuged with an applied 1g force. The mg units were place in the static positions for continued mg exposure. After 30 minutes of pre-incubation, mg non-activated units were fixed by addition of RNALater (QIAGEN, Valencia, CA), removed from the incubator, and stored in 4M-BM-0C. The mg and 1g activated units were injected with final concentration 10mg/ml Con A and 4mg/ml anti-CD28. These cassettes were replaced into KUBIK on either the centrifuge or static positions and activated for 1.5 hours. Activation was stopped with the addition of RNALater and the units were then moved to 4M-BM-0C storage. All units were returned to Earth for analysis.
2012-06-20 | E-GEOD-38836 | biostudies-arrayexpress
Project description:Gene expression profile of CAR T cells compared to control ΔCAR T cells
| PRJNA451003 | ENA
Project description:Nanostring analysis of human SUV39H1-knockout CAR T compared to control CAR T cells (mock) at different timepoint
| PRJNA1021138 | ENA
Project description:Compared the gene expression profiles between the PTL-Her2-CAR-T cells and Her2-CAR-T cells isolated from tumor tissues
| PRJNA542661 | ENA
Project description:Chimeric antigen receptor (CAR) T cells have revolutionized the landscape of cancer therapy, demonstrating unprecedented success in treating relapsed or refractory blood cancers. Previous studies of the mechanisms underlying the interactions and responses of CAR T cells and their targets have focused on the activation of CAR T cells and attempted to optimize CAR design to increase efficacy, while ignoring tumors and their responses to CAR ligation. We evaluated the signaling of a second-generation, ligand-based CAR built from the colony-stimulating factor 1 (CSF1) ligand to target the CSF1 receptor (CSF1R) on CSF1R-expressing target cells, and compared it to a conventional single-chain variable fragment (scFv)–based CAR against the B-cell antigen CD19 using stable isotope labeling by amino acids in cell culture (SILAC) co-culture with phosphotyrosine (pY) enrichment and liquid chromatography–tandem mass spectrometry (LC–MS/MS).. We showed that ligation of CSF1R-expressing THP-1 cells with CSF1R-CAR T cells stimulated CSF1R-like signaling in the THP-1 cells, whereas no target cell signaling response was observed after the ligation of CD19-CAR T cells with target Raji cells. In experiments with small-molecule inhibitors of the tyrosine kinase Lck, actin polymerization, and CSF1R, we found that CAR-induced CSF1R signaling in THP-1 cells depended exclusively on the kinase activity of CSF1R with no participation from T cell activation. Consistently, CSF1R-CAR T cells promoted THP-1 cell growth at low effector-to-target (E:T) ratios but prevented THP-1 cell growth at high E:T ratios. Our data provide evidence for an unintended consequence of CARs: CAR-induced signaling in cancer cells. These data may have broad implications for the choice of CAR antigen for optimal clinical efficacy.
2025-11-21 | PXD058576 | Pride
Project description:Purpose: Compared the differences in the transcriptome of T cells versus EpCAM CAR-T cells and EpCAM CAR-T cells versus rapamycin-pretreated EpCAM CAR-T cells.Methods: Next-generation sequencing (NGS) has revolutionized the systems-based analysis of cellular pathways. The goals of this study are to compare NGS-derived transcriptome profiling (RNA-seq) between T cells and EpCAM CAR-T cells，and between EpCAM CAR-T cells and rapamycin-pretreated EpCAM CAR-T cells. Results: RNA-seq showed that CAR-T cells significantly upregulated the expression of exhaustion markers compared to T cells. Gene Set Enrichment Analysis (GSEA) analysis showed that CAR-T cells cells were enriched for signatures of apoptosis. Compared with T cells, Kyoto Encyclopedia of Genes and Genomessignaling(KEGG) pathway analysis showed that the PI3K/AKT/mTOR signaling pathway was significantly enriched. Likewise, GSEA showed that the mTOR signaling pathway was significantly upregulated in CAR-T cells. Next, we analyzed the RNA-seq data between CAR-T cells and rapamycin-pretreated CAR-T cells. RNA-seq showed that rapamycin-treated CAR T down-regulated the expression of exhaustion markers compared with untreated CAR-T cells. GSEA analysis showed that the apoptosis-related gene set was enriched in untreated CAR-T cells.Conclusions:In vitro culture promotes the terminal differentiation of CAR-T cells.CAR-T cells present a highly activated mTOR phenotype. Rapamycin pretreatment prevents CAR-T cells terminal differentiation.
2021-12-05 | GSE162796 | GEO
Project description:Gene expression profile of SmarT-cells compared to control T cells modified to express ΔCAR, ΔTGFbRII and ΔIL4R
| PRJNA451005 | ENA