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Epigenetic checkpoint regulates anti-tumor immunity of CD4 T cell in Hepatocellular carcinoma

ABSTRACT: Epigenetic checkpoint regulates anti-tumor immunity of CD4 T cell in Hepatocellular carcinoma

PROVIDER: PRJNA981474 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24875715_1.fastq.gz	Fastqsanger.gz
	SRR24875715_2.fastq.gz	Fastqsanger.gz
	SRR24875716_1.fastq.gz	Fastqsanger.gz
	SRR24875716_2.fastq.gz	Fastqsanger.gz
	SRR24875717_1.fastq.gz	Fastqsanger.gz

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Epigenetic checkpoint regulates anti-tumor immunity of CD4 T cell in Hepatocellular carcinoma

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Fucosylation of HLA-DRB1 regulates CD4+T cell-mediated anti-melanoma immunity and enhances immunotherapy efficacy: CD4+ T Cell Phosphoproteomics

Project description:Immunotherapy efficacy is limited in melanoma, and combinations of immunotherapies with other modalities have yielded limited improvements but also adverse events requiring cessation of treatment. In addition to ineffective patient stratification, efficacy is impaired by paucity of intratumoral immune cells (itICs)—thus, effective strategies to safely increase itICs are needed. We report that dietary administration of L-fucose induces fucosylation and cell surface enrichment of the MHC-II protein HLA-DRB1 in melanoma cells, triggering CD4+T cell-mediated increases in ItICs and anti-tumor immunity, enhancing immune checkpoint blockade responses. Melanoma fucosylation and fucosylated HLA-DRB1 associate with intratumoral T cell abundance and anti-PD1 responder status in patient melanoma specimens, suggesting the potential use of melanoma fucosylation as a strategy for stratifying patients for immunotherapies. Our findings demonstrate that fucosylation is a key mediator of anti-tumor immunity, and importantly, suggest that L-fucose is a powerful agent for safely increasing ItICs and immunotherapy efficacy in melanoma.

2022-12-16 | PXD038065 | Pride

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LSD1 ablation stimulates anti-tumor immunity and enables checkpoint blockade

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Targeting ERAP enhances anti-tumor immunity by disrupting the NKG2A/HLA-E inhibitory checkpoint

Project description:New targets that enhance anti-tumor immunity must be identified to improve the efficacy of cancer immunotherapy. Here we show that loss of endoplasmic reticulum aminopeptidase (ERAP) family proteins improves anti-tumor immunity and synergizes with immune checkpoint blockade. Mechanistically, we show that loss of ERAP inactivates the HLA-E/NKG2A checkpoint, which normally restrains tumor killing by both CD8+ T cells and NK cells. The inhibitory activity of HLA-E is dependent on its presentation of a restricted set of invariant epitopes which form the binding surface for the NKG2A/CD94 receptor complex. Using genetic screening, in vivo models, cell-based assays, and immunopeptidomics, we show that loss of ERAP activity prevents the processing of these invariant peptides and alters the presented peptidome of both HLA-E and classical MHC-I. HLA-E neo-peptides presented after ERAP deletion are unable to bind the NKG2A/CD94 receptor, rendering tumor cells highly susceptible to killing by NKG2A+ cytotoxic T and NK cells. Thus, loss of ERAP phenocopies the loss or inhibition of the HLA-E/NKG2A pathway and represents an attractive therapeutic approach to inhibit this critical checkpoint. More broadly, this work identifies ERAP1/2 as druggable intracellular enzymes that could be targeted using small molecules to inactivate a cell-surface inhibitory pathway and represents a novel approach to therapeutic modulation of immune responses.

2024-11-21 | PXD052031 | Pride

Epigenetic checkpoint regulates anti-tumor immunity of CD4 T cell in Hepatocellular carcinoma II

Project description:To investigated how CD4 T cells change in the development of hepatocelluar carcinoma We then performed gene expression profiling analysis using data obtained from RNA-seq of CD4 T cells

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