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Crosslinking of Ly6a metabolically reprograms CD8 T cells for cancer immunotherapy.

ABSTRACT: Crosslinking of Ly6a metabolically reprograms CD8 T cells for cancer immunotherapy.

PROVIDER: PRJNA1139138 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29928533.fastq.gz	Fastqsanger.gz
	SRR29928534.fastq.gz	Fastqsanger.gz
	SRR29928535.fastq.gz	Fastqsanger.gz
	SRR29928536.fastq.gz	Fastqsanger.gz
	SRR29928537.fastq.gz	Fastqsanger.gz

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Crosslinking of Ly6a metabolically reprograms CD8 T cells for cancer immunotherapy.

Project description:T cell inhibitory mechanisms prevent autoimmune reactions, while cancer immunotherapy aims to remove these inhibitory signals, Chronic UV exposure attenuates autoimmunity through promotion of unknown immune-suppressive mechanisms. Here we showed that mice with subcutaneous melanoma were not responsive to anti-PD1 immunotherapy following chronic UV irradiation, given prior to tumor injection, due to the suppression of T cell killing ability in skin-draining lymph nodes. Using mass cytometry and single-cell RNA-sequencing analyses, we discovered that skin-specific, UV-induced suppression of T-cells killing activity is mediated by upregulation of Ly6ahigh T-cells subpopulation. Independently of the UVB effect, Ly6ahigh T cells were induced by chronic type-1 interferon in the tumor microenvironment. Treatment with an anti-Ly6a antibody enhanced the anti-tumoral cytotoxic activity of T cells and reprogrammed their mitochondrial metabolism via the Erk/cMyc axis. Remarkably, treatment with anti-Ly6a antibody significantly inhibited tumor growth in mice resistant to anti-PD1 therapy. Applying our findings in humans could lead to a new immunotherapy treatment for patients with resistance to existing treatments.

2024-08-04 | GSE272861 | GEO

Crosslinking of Ly6a metabolically reprogram CD8 T cells for cancer immunotherapy.

Project description:To evaluate the downstream effects of anti-Ly6a crosslinking, we examined the effect of anti-Ly6a antibodies on CD8+ T cell activity in the presence and absence of target tumor cells by high-resolution mass spectrometry proteomic analyses. Spleen cells were isolated from gp10025–33 TCR transgenic mice and incubated for 3 days with IL-2, IFNα, and gp10025–33 peptide. Next, CD8+ T-cells were isolated and incubated overnight with anti-Ly6a antibody (or IgG with or without B16F10 melanoma cells. CD8+ T-cells were then sorted and subjected to proteomic analysis using high-resolution mass spectrometry

2024-08-04 | PXD050734 | Pride

Crosslinking of Ly6a metabolically reprograms CD8 T cells for cancer immunotherapy.

Project description:T cell inhibitory mechanisms prevent autoimmune reactions, while cancer immunotherapy aims to remove these inhibitory signals. Chronic ultraviolet (UV) exposure attenuates autoimmunity through promotion of poorly understood immune-suppressive mechanisms. Here we show that mice with subcutaneous melanoma are not responsive to anti-PD1 immunotherapy following chronic UV irradiation, given prior to tumor injection, due to the suppression of T cell killing ability in skin-draining lymph nodes. Using mass cytometry and single-cell RNA-sequencing analyzes, we discover that skin-specific, UV-induced suppression of T-cells killing activity is mediated by upregulation of a Ly6ahigh T-cell subpopulation. Independently of the UV effect, Ly6ahigh T cells are induced by chronic type-1 interferon in the tumor microenvironment. Treatment with an anti-Ly6a antibody enhances the anti-tumoral cytotoxic activity of T cells and reprograms their mitochondrial metabolism via the Erk/cMyc axis. Treatment with an anti-Ly6a antibody inhibits tumor growth in mice resistant to anti-PD1 therapy. Applying our findings in humans could lead to an immunotherapy treatment for patients with resistance to existing treatments.

| S-EPMC11437002 | biostudies-literature

Octopamine metabolically reprograms astrocytes to confer neuroprotection against α-synuclein

Project description:Octopamine metabolically reprograms astrocytes to confer neuroprotection against α-synuclein

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Microbial cancer immunotherapy reprograms hematopoiesis to enhance myeloid-driven anti-tumor immunity [Human_Mulitome_Cohort1]

Project description:Mycobacterium bovis Bacillus Calmette-Guérin (BCG) is the vaccine against tuberculosis and an immunotherapy for bladder cancer. When administered intravenously, BCG reprograms bone marrow hematopoietic stem and progenitor cells (HSPCs), leading to heterologous protection against infections. Whether HSPC reprogramming contributes to the anti-tumor effects of BCG administered into the bladder is unknown. We demonstrate that BCG administered in the bladder colonizes the bone marrow and, in both mice and humans, reprograms HSPCs to alter and amplify myelopoiesis. BCG-reprogrammed HSPCs are sufficient to confer augmented anti-tumor immunity through production of neutrophils, monocytes, and dendritic cells that broadly remodel the tumor microenvironment, drive T cell-dependent anti-tumor responses, and synergize with checkpoint blockade. We conclude that bladder BCG acts systemically through hematopoiesis, highlighting the broad potential of HSPC reprogramming to enhance the innate drivers of T cell-dependent tumor immunity.

2025-04-22 | GSE295277 | GEO

Microbial cancer immunotherapy reprograms hematopoiesis to enhance myeloid-driven anti-tumor immunity [Human_Multiome_Cohort2

2025-04-22 | GSE295308 | GEO

Microbial cancer immunotherapy reprograms hematopoiesis to enhance myeloid-driven anti-tumor immunity [Mouse_Multiome]

2025-04-22 | GSE295006 | GEO

Microbial cancer immunotherapy reprograms hematopoiesis to enhance myeloid-driven anti-tumor immunity [Mouse_LSK_ATAC]

2025-04-22 | GSE295004 | GEO

Microbial cancer immunotherapy reprograms hematopoiesis to enhance myeloid-driven anti-tumor immunity [Mouse_CD45_scRNA]

2025-04-22 | GSE295003 | GEO

Targeting METTL3 reprograms tumor microenvironment to improve cancer immunotherapy [RNA-seq]

Project description:Targeting METTL3 reprograms tumor microenvironment to improve cancer immunotherapy [RNA-seq]

| PRJNA874419 | ENA