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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

Octopamine metabolically reprograms astrocytes to confer neuroprotection against α-synuclein

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

| PRJNA882845 | ENA

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

Schistosoma mansoni infection metabolically reprograms the myeloid lineage in a mouse model of metabolic disease

Project description:Schistosoma mansoni infection metabolically reprograms the myeloid lineage in a mouse model of metabolic disease

| PRJNA648919 | ENA

Pro-survival Lipid Sphingosine-1-Phosphate Metabolically Reprograms T cell to Limit its Anti-Tumor Activity

Project description:Pro-survival Lipid Sphingosine-1-Phosphate Metabolically Reprograms T cell to Limit its Anti-Tumor Activity

| PRJNA531482 | ENA

SHISA3 reprograms tumor-associated macrophages toward an M1 phenotype and enhances cancer immunotherapy

Project description:SHISA3 reprograms tumor-associated macrophages toward an M1 phenotype and enhances cancer immunotherapy

| PRJNA1076213 | ENA

Maternal slimming reprograms metabolic gene expression in mice offspring

Project description:This SuperSeries is composed of the following subset Series: GSE40471: Maternal slimming reprograms metabolic gene expression in mice offspring (NimbleGen expression) GSE40477: Maternal slimming reprograms metabolic gene expression in mice offspring (NimbleGen methylation) GSE40478: Maternal slimming reprograms metabolic gene expression in mice offspring (mRNA-Seq) Refer to individual Series

2012-08-30 | E-GEOD-40479 | biostudies-arrayexpress

Ex vivo activation of the GCN2 pathway metabolically reprograms T cells leading to enhanced adoptive cell therapy

Project description:Ex vivo activation of the GCN2 pathway metabolically reprograms T cells leading to enhanced adoptive cell therapy

| PRJNA1074242 | ENA

A phosphatase-like nanomaterial promotes autophagy and reprograms macrophage for cancer immunotherapy

Project description:Macrophages are very plastic and play key roles in maintenance of tissue homeostasis. In cancer progression, macrophages also take parts through all the processes, from the initiation, progression, to the final tumor metastasis. Although energy deprivation and autophagy are widely used for cancer therapy, most of these strategies are not meant to target macrophages resulting in undesired effects and unsatisfactory outcomes for cancer immunotherapy. Herein, we developed a lanthanum nickel oxide (LNO) nanozyme that possesses phosphatase-like activity for ATP hydrolysis. Meanwhile, the autophagy of macrophages induced by LNO promotes the polarization of macrophages from M2-like macrophage (M2) to M1-like macrophage (M1) and reduces tumor-associated macrophages in tumor-bearing mice, exhibiting capability of killing tumor-associated macrophage and anti-tumor effect in vivo. Furthermore, pre-coating by myeloid cell membrane on the surface of LNO significantly enhanced antitumor immunity. Our findings demonstrate that phosphatase-like nanozyme, LNO can specifically induce macrophage autophagy that improves therapeutic efficacy and offers valuable strategies for cancer immunotherapy.

2024-08-10 | PXD051695 | Pride

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