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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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IFN-γ Upregulates Survivin and Ifi202 Expression to Induce Survival and Proliferation of Tumor-Specific T Cells

ABSTRACT: Transcriptional profiling of mouse tumor-specific cytotoxic T lymphocytes (CTL) comparing activation-induced gene expression profiles induced by tumor-specific antigen (Ag) and CD3 mAb. CTLs were stimulated with either Ag or CD3 mAb for 3 and 24 h, respectively. The stimulated CTLs were compared to un-stimulated CTLs. The objective was to identify differential gene expression profiles induced by the two activation (Ag vs CD3 mAb) conditions. Two-condition experiments, un-stimulated vs stimulated CTLs. Biological replicates: 3 replicates for each comparison. Unstimulated CTLs were compared to stimulated CTLs (Ag and CD3 mAb, respectively).

ORGANISM(S): Mus musculus

SUBMITTER: Kebin Liu

PROVIDER: E-GEOD-22890 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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IFN-γ upregulates survivin and Ifi202 expression to induce survival and proliferation of tumor-specific T cells.

Zimmerman Mary M Yang Dafeng D Hu Xiaolin X Liu Feiyan F Singh Nagendra N Browning Darren D Ganapathy Vadivel V Chandler Phillip P Choubey Divaker D Abrams Scott I SI Liu Kebin K

PloS one 20101122 11

<h4>Background</h4>A common procedure in human cytotoxic T lymphocyte (CTL) adoptive transfer immunotherapy is to expand tumor-specific CTLs ex vivo using CD3 mAb prior to transfer. One of the major obstacles of CTL adoptive immunotherapy is a lack of CTL persistence in the tumor-bearing host after transfer. The aim of this study is to elucidate the molecular mechanisms underlying the effects of stimulation conditions on proliferation and survival of tumor-specific CTLs.<h4>Methodology/principal ...[more]

PMID: 21124930

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IFN-γ Upregulates Survivin and Ifi202 Expression to Induce Survival and Proliferation of Tumor-Specific T Cells

Project description:Transcriptional profiling of mouse tumor-specific cytotoxic T lymphocytes (CTL) comparing activation-induced gene expression profiles induced by tumor-specific antigen (Ag) and CD3 mAb. CTLs were stimulated with either Ag or CD3 mAb for 3 and 24 h, respectively. The stimulated CTLs were compared to un-stimulated CTLs. The objective was to identify differential gene expression profiles induced by the two activation (Ag vs CD3 mAb) conditions.

2010-12-03 | GSE22890 | GEO

RNA-seq of murine cytotoxic T lymphocytes unstimulated and stimulated with anti-CD3 for 10, 20, 40 and 60 minutes

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2023-10-15 | E-MTAB-12083 | biostudies-arrayexpress

Gene-expression profiles of PD-L1-affected CD8+ T cells

Project description:Programmed cell death 1 ligand 1 (PD-L1) is known to suppress immune system and to be an unfavorable prognostic factor in ovarian cancer. The purpose of this study was to elucidate the function of PD-L1 in peritoneal dissemination. Tumor cell lysis by CTLs was attenuated when PD-L1 on tumor cells was overexpressed and promoted when it was silenced. PD-L1 overexpression also inhibited gathering and degranulation of CTLs. Gene expression profile of mouse CTLs caused by PD-L1-overexpressing ovarian cancer was related to human CTLs exhaustion. In mouse ovarian cancer dissemination models, depleting PD-L1 expression on tumor cells resulted in inhibited tumor growth in the peritoneal cavity and prolonged survival. Restoring immune function by inhibiting immune-suppressive factors such as PD-L1 may be a promising therapeutic strategy for peritoneal dissemination. Genome-wide transcriptional changes in OT-1 mouse CD8+ T cells that were co-incubated with OVA peptide-loaded ID8 mouse ovarian cancer cell lines. CTLs from 4 mice were devided into 2 groups, and co-incubated with PD-L1-overexpressed ID8 or PD-L1-depleted ID8.

2012-07-09 | E-GEOD-39205 | biostudies-arrayexpress

RNA-seq of effector (CD43+) CD8+ T cells, CD45+ hematopoietic cells and CD45- tumor/stromal cells from mice bearing bilateral AT-3 tumors following radio-immunotherapy of which one tumor was irradiated

Project description:Radiotherapy (RT) destroys tumor cells, which may lead to release of antigens and immune-activating signals. In this way, RT may act as an in situ vaccine and kick-start a T-cell response against the tumor. Immunotherapy enhances tumor-specific T-cell responses. Combination of radiotherapy and immunotherapy (radio-immunotherapy (RIT)) can therefore be expected to synergize in inducing and sustaining systemic anti-tumor T-cell responses. However, in the clinic, systemic combined responses between radiotherapy and immunotherapy are rarely observed, as the effect of RIT combinations on ‘abscopal’ tumors outside the radiotherapy field are not (yet) greater than the effect of immunotherapy alone. In order to define potential bottlenecks in the tumor micro-environment that impede CD8 T cell activity, we harvested irradiated and non-irradiated tumors from the same mice that were treated with RIT (10 Gy RT, anti-CD137 and anti-PD1). From these tumors, effector (CD43+) CD8 T cells, ‘other’ hematopoietic (CD45+) cells and tumor/stromal (CD45-) were sorted and RNA sequencing was performed to identify differences between these cell populations in the irradiated and non-irradiated tumors that could explain the lack of T cell activity in the non-irradiated tumor.

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Actinomycin D treated cytotoxic T lymphocytes

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2023-10-16 | PXD034920 | Pride

CD6 co-stimulation of human peripheral blood mononuclear cells

Project description:Difference in gene expression profile between 30000 freshly isolated human PBMCs stimulated with the immobilized anti-CD3 mAb (0.25µg/ml) alone (lane 1), along with ALCAM-Fc (1µg/ml) (lane 2), IL-2 (2.5ng/ml) (lane 4) or both (lane 3) or compared to unstimulated cells (lane 5), incubated for 72 h.

2009-05-30 | GSE16331 | GEO

Proteome of WT and Usp30KO cytotoxic T lymphocytes

Project description:Recent work in immunometabolism has emphasised the role of mitochondria in both the innate and adaptive immune system. Mitochondria are important in T cell development and differentiation, but less is known about their role in CD8+ effector T cells (CTLs). We found that CTLs that lack the mitochondrial deubiquitinase USP30 undergo promiscuous mitophagy, destroying most of the cellular mitochondria. Surprisingly, this results in a markedly diminished killing capacity, while motility, signalling and secretion remain intact. This study uses quantitative DIA proteomics to measure the impact of USP30 deficiency on the global proteome of IL-2 maintained, 4.5 h TCR retriggered and 4.5 h TCR retriggered + cycloheximide CTL. Unexpectedly, inhibition of mitochondrial translation, through genetic or pharmacologic methods, was the mechanism by which CTL killing was impaired. Reduced mitochondrial translation triggered attenuated cytosolic translation which precluded replenishment of secreted effector molecules thereby limiting the capacity of CTLs to serially kill multiple targets. Thus, mitochondria emerge as a previously unappreciated homeostatic regulator of protein translation required for serial CTL killing.

2022-06-09 | PXD021508 | Pride

CD6 co-stimulation of human peripheral blood mononuclear cells

Project description:Difference in gene expression profile between 30000 freshly isolated human PBMCs stimulated with the immobilized anti-CD3 mAb (0.25Âµg/ml) alone (lane 1), along with ALCAM-Fc (1Âµg/ml) (lane 2), IL-2 (2.5ng/ml) (lane 4) or both (lane 3) or compared to unstimulated cells (lane 5), incubated for 72 h. Organism used: Human Slides: Human 8x15k Arrays Starting material: Human peripheral blood mononuclear cells RNA Samples used: Pooled 1 â Unstimulated, Anti-CD3, Anti-CD3 + IL-2, Anti-CD3 + ALCAM, Anti-CD3 +ALCAM + IL-2. Labeling kit: Agilentâs Quick-Amp labeling Kit (p/n5190-0444) Labeling Method: T7 promoter based-linear amplification to generate labeled complementary RNA (One-Color Microarray-Based Gene Expression Analysis) Total RNA and cRNA Purification Kit: Hybridization Kit: Qiagenâs RNeasy minikit Cat#74104 RNA quality was checked using Bioanalyzer.

2010-05-18 | E-GEOD-16331 | biostudies-arrayexpress

Gene expression profile of regenerated CD8αα T cells and CD8αβ T cells from LMP2 T-iPSCs

Project description:Whereas cytotoxic T lymphocytes (CTLs) represent the most promising therapeutic avenue in cancer immunotherapy, adaptive transfer of antigen-specific CTLs has faced difficulty in efficient expansion of CTLs from patients in ex vivo culture. To solve this issue, several groups have proposed that the induced pluripotent stem cell (iPSC) technology can be applied for the expansion of antigen-specific CTLs: when iPSCs are produced from antigen-specific CTLs and CTLs are induced from these iPSCs, all regenerated CTLs express the same TCR as original CTLs. However, in these previous studies, one critical issue remains to be solved. With current methods, the regenerated CTLs are mostly of the CD8αα+ innate type and have less antigen-specific cytotoxic activity than primary CTLs. Here we report that, by stimulating purified iPSC-derived CD4/CD8 double positive (DP) cells with anti-CD3 antibody, T cells expressing CD8αβ were generated and they had cytotoxic activity comparable to primary CTLs.

2016-11-15 | GSE81975 | GEO

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Project description:We have employed whole genome microarray expression profiling of human Treg and Tconv cells as a discovery platform to identify genes differentially expressed upon signal of pseudostarvation (either mTOR inhibition or leptin neutralizaion) responsible for proliferation of Treg cell on one side and inhibition of Tconv cells on the other. Human Treg and Tconv cells isolated from healthy donors were pretreated or not with rapamycin or leptin mAb and stimulated with anti-CD3 and anti-CD28 beads for 12h.

2021-05-17 | GSE154401 | GEO

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