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Epigenetic therapy strengthens immune synapses to potentiate susceptibility of lung cancer cells to adoptive γδ T cell therapy [seq]

ABSTRACT: Epigenetic therapy strengthens immune synapses to potentiate susceptibility of lung cancer cells to adoptive γδ T cell therapy [seq]

PROVIDER: PRJNA607909 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11130922.fastq.gz	Fastqsanger.gz
	SRR11130923.fastq.gz	Fastqsanger.gz
	SRR11130924_1.fastq.gz	Fastqsanger.gz
	SRR11130924_2.fastq.gz	Fastqsanger.gz
	SRR11130925_1.fastq.gz	Fastqsanger.gz

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Epigenetic therapy strengthens immune synapses to potentiate susceptibility of lung cancer cells to adoptive γδ T cell therapy

Project description:Epigenetic therapy strengthens immune synapses to potentiate susceptibility of lung cancer cells to adoptive γδ T cell therapy

| PRJNA607906 | ENA

Epigenetic therapy strengthens immune synapses to potentiate susceptibility of lung cancer cells to adoptive γδ T cell therapy

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-02-16 | GSE145664 | GEO

Epigenetic therapy strengthens immune synapses to potentiate susceptibility of lung cancer cells to adoptive γδ T cell therapy [seq]

Project description:Purpose: Epigenetic drug DNA methyltransferase inhibitors (DNMTis) are immunomodulating agents that may sensitize cancer cells to immune cell attack. However, it is still unclear how DNMTi affects cancer cells to the killing by immune cells. We therefore try to uncover the alternations of genomic DNA methylation, chromatin accessibility and transcriptomes after DNMTi treatment of cancer cells. Methods: Six human lung cancer cell lines (A549, H1299, CL1-0, CL1-5, H1792, PC9) treated without (Mock) or with 100 nM decitabine (DAC) for 72 hours followed by growing in drug-free medium for three days were subjected to mRNA-seq and Omni-ATAC-seq analyses. Results: mRNA-seq and ATAC-seq analyses reveal upregulation of actin and intermediate filament, and downregulation of microtubule modules by decitabine in human lung cancer cell lines. Conclusion: Decitabine primes lung cancer cells to γδ T cell-mediated killing through regulating cytoskeleton associated genes potentially involved in immune synapse formation.

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Adoptive cell therapy [Fig.4]

Project description:Adoptive cell therapy [Fig.4]

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Metabolic conditioning of CD8+ effector T cells for adoptive cell therapy

Project description:Metabolic conditioning of CD8+ effector T cells for adoptive cell therapy

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Dendritic cell ICAM-1 strengthens synapses of CD8 T cells and dendritic cells but is dispensable for effector and memory responses

Project description:Dendritic cell ICAM-1 strengthens synapses of CD8 T cells and dendritic cells but is dispensable for effector and memory responses

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Metabolic conditioning of CD8+ effector T cells for adoptive cell therapy

Project description:Effector CD8+ T cell (TE) proliferation and cytokine production depends on enhanced glucose metabolism. However, circulating T cells continuously adapt to glucose fluctuations caused by diet and inter-organ metabolite exchange. Here we show that transient glucose restriction (TGR) in activated CD8+ TE metabolically primes effector functions and enhances tumour clearance in mice. Tumor-specific TGR CD8+ TE co-cultured with tumor spheroids in replete conditions display enhanced effector molecule expression, and adoptive transfer of these cells in a murine lymphoma model leads to greater numbers of immunologically functional circulating donor cells and complete tumor clearance. Mechanistically, TGR TE undergo metabolic remodelling that upon glucose re-exposure supports enhanced glucose uptake, increased carbon allocation to the pentose phosphate pathway (PPP), and a cellular redox shift toward a more reduced state, all indicators of a more anabolic program to support their enhanced functionality. Thus, metabolic conditioning could be utilized to promote efficiency of T cell products for adoptive cellular therapy.

2020-08-03 | GSE152018 | GEO

Adoptive cell therapy across cancer diagnoses

Project description:Primary objectives: The main objective is to determine the feasibility and safety of adoptive cell therapy in combination with checkpoint inhibition across different metastatic solid cancers. Primary endpoints: Toxicity: Registration of all AEs and unexpected events in relation to the treatment will be done in accordance with the common terminology criteria for adverse events (CTCAE) criteria as described in appendix 3.

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LSD1 inhibition improves efficacy of adoptive T cell therapy by enhancing CD8+ T cell responsiveness

Project description:The lysine-specific histonedemethylase1A(LSD1) has been described to play a role in antitumor immunity; however, the role of LSD1 in shaping CD8+ T cell (CTL) differentiation and function is not understood. Here, we showed that pharmacological inhibition of LSD1 (LSD1i) in CTL elicited phenotypic and functional alterations of the CTL that led to robust antitumor immunity in the context of adoptive T cell therapy (ACT). In addition, the combination of anti-PDL1 therapy with LSD1i-based ACT resulted in a complete tumor eradication and long-lasting tumor-free survival. This study demonstrated that LSD1i together with anti-PDL1 therapy complement each other’s deficiencies and produce a better tumor response in a melanoma model, in which both immune and epigenetic therapy alone have shown limited efficacy. Collectively, these results set the translational potential of modulating LSD1 to improve antitumoral responses generated by ACT and anti-PDL1 therapy, which provide a strong rationale for a combination trial of LSD1i and immunotherapy.

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Epigenetic Suppression of Transgenic T-cell Receptor Expression via Gamma-Retroviral Vector Methylation in Adoptive Cell Transfer Therapy

Project description:Transgenic T-cell receptor (TCR) adoptive cell therapies recognizing tumor antigens are associated with robust initial response rates, but frequent disease relapse. This usually occurs in the setting of poor long-term persistence of cells expressing the transgenic TCR, generated using murine stem cell virus (MSCV) -retroviral vectors. Analysis of clinical transgenic adoptive cell therapy products in vivo revealed that despite strong persistence of the transgenic TCR DNA sequence over time, its expression was profoundly decreased over time at the RNA and protein levels. Patients with the greatest degrees of expression suppression displayed significant increases in DNA methylation over time within the MSCV promoter region, as well as progressive increases in DNA methylation within the entire MSCV vector over time. These increases in vector methylation occurred independently of its integration site within the host genomes. These results have significant implications for the design of future viral-vector gene engineered adoptive cell transfer therapies.

2020-07-06 | GSE153820 | GEO

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