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Atractylenolide I enhances responsiveness to immune checkpoint blockade therapy by activating tumor antigen presentation

ABSTRACT: Atractylenolide I enhances responsiveness to immune checkpoint blockade therapy by activating tumor antigen presentation

PROVIDER: PRJNA718568 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14108373.fastq.gz	Fastqsanger.gz
	SRR14108374.fastq.gz	Fastqsanger.gz
	SRR14108375.fastq.gz	Fastqsanger.gz
	SRR14108376.fastq.gz	Fastqsanger.gz
	SRR14108377.fastq.gz	Fastqsanger.gz

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Atractylenolide I enhances responsiveness to immune checkpoint blockade therapy by activating tumor antigen presentation

Project description:One of the primary mechanisms of tumor cell immune evasion is the loss of antigenicity, which arises due to lack of immunogenic tumor antigens as well as dysregulation of the antigen processing machinery. In a screen for small-molecule compounds from herbal medicine thatpotetiate T cell-mediated cytotoxicity, we identified atractylenolide I (ATT-I) that significantly promotes tumor antigen presentation of both human and mouse colorectal cancer (CRC) cells and thereby enhances the cytotoxic response of CD8+ T cells. Cellular thermal shift assay (CETSA) with multiplexed quantitative mass spectrometry identified the proteasome 26S subunit non-ATPase 4 (PSMD4), an essential component of the immunoproteasome complex,as a primary target protein of ATT-I. Binding of ATT-I with PSMD4 augments the antigenprocessing activity of immunoproteasome, leading to enhanced major histocompatibility class I(MHC-I)-mediated antigen presentation on cancer cells. In syngeneic mouse CRC models and human patient-derived CRC organoid models, ATT-I treatment promotes the cytotoxicity of CD8+ T cells and thus profoundly enhances the efficacy of immune checkpoint blockade therapy. Collectively, we show here that targeting the function of immunoproteasome with ATT-I promotes tumor antigen presentation, empowers T-cell cytotoxicity, and thus elevates the tumorresponse to immunotherapy.

2021-03-31 | GSE171158 | GEO

Resistance to Checkpoint Blockade Therapy Through Inactivation of Antigen Presentation

Project description:Resistance to Checkpoint Blockade Therapy Through Inactivation of Antigen Presentation

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Ferroptotic tumor cells revamp tumor-associated macrophage antigen presentation to unleash immune checkpoint blockade efficacy

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Atractylenolide I enhances responsiveness to immune checkpoint blockade therapy by activating tumor antigen presentation.

Project description: Not available

| S-EPMC8121519 | biostudies-literature

Senescence prostate cancer cell promotes resistance to immune checkpoint blockade through ATR activation

Project description:Background: Checkpoint blockade immunotherapy represented by PD-1/PD-L1 or CTLA4 antibody treatment, has been of tremendous success for multiple cancers. Most patients with prostate cancer (PCa) either do not respond to CTLA4 immune checkpoint blockade or develop resistance to it, often because of low CTLA4 antigen presentation in cancer cells.

2025-04-02 | GSE234387 | GEO

Distinct Stemness Programs and PD-1 Responsiveness of Progenitor Exhausted CD8+ T Cells between Chronic Viral Infection and Tumor

Project description:We reported the CD8+ T cell exhaustion differences between chronic viral infection and tumor regarding their transcriptomic and epigenetic landscapes, immune checkpoint blockade responsiveness and underlying molecular mechanisms by using single-cell RNA-seq.

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Disease-specific exhaustion features and PD-1 immunotherapy responsiveness of antigen-specific CD8+ T cells at single-cell resolution [scRNA-seq]

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γδ T cells are effectors of immunotherapy in cancers with HLA class I defects

Project description:DNA mismatch repair deficient (MMR-d) cancers present an abundance of neoantigens that likely underlies their exceptional responsiveness to immune checkpoint blockade (ICB). However, MMR-d colon cancers that evade CD8+ T cells through loss of Human Leukocyte Antigen (HLA) class I-mediated antigen presentation frequently remain responsive to ICB, suggesting the involvement of other immune effector cells.

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Anti-tumor immunity induces the presentation of aberrant peptides in melanoma

Project description:Extensive tumor inflammation, reflected by high levels of infiltrating T-cells and Interferon gamma (IFNγ) signaling, is thought to improve checkpoint immunotherapy response. However, many tumors escape by activating multiple cellular pathways that induce immunosuppression. One pivotal immune-suppressive mechanism is the production of Tryptophan metabolites along the kynurenine pathway by IFNγ-induced IDO1 enzyme production. However, phase III clinical trials using chemical inhibition of IDO1 in combination with PD1 pathway blockade failed to improve melanoma treatment, suggesting incomplete understanding of the role of IDO1 and the consequent Tryptophan degradation on mRNA translation and cancer progression. Here, we investigated the effects of prolonged IFNγ treatment on mRNA translation in melanoma cells by ribosome profiling. Our results suggest that IFNγ-induced IDO1-mediated Tryptophan depletion may play a key role in the immune recognition of melanoma cells, by inducing the production and presentation of aberrant peptides.

2020-10-18 | GSE142822 | GEO

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