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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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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

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

Project description: Not available

| S-EPMC8121519 | biostudies-literature

Resistance to Checkpoint Blockade Therapy Through Inactivation of Antigen Presentation

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

| PRJNA398303 | ENA

Resistance to checkpoint blockade therapy through inactivation of antigen presentation.

Project description: Not available

| S-EPMC5656607 | biostudies-literature

Preclinical model of anti-PDL1 Immune-checkpoint blockade (ICB) resistance in breast cancer associated to low antigen presentation machinery (APM)

Project description:Immune-checkpoint blockade (ICB) immunotherapy has emerged as one of the most effective therapies in oncology by unleashing anti-tumor response. However, despite the improvement in the clinical outcome of TNBC patients, most patients do not respond yet. Thus, to understand the underlying mechanisms of ICB resistance is necessary. With this purpose, we generated a preclinical immunocompetent syngeneic model of anti-PD-L1 ICB resistance. Mouse breast cancer 4TO7 cells were orthotopically implanted by MFP and at 0.5 x 0.5 cm tumor size mice were treated with anti-PD-L1 (10mg/Kg every 3 days). Though tumors initially responded, they eventually developed resistance to anti-PD-L1 treatment. Immunotherapy resistant tumor (IRT) cells and control tumor cells were isolated and validated again for anti-PDL1 resistance in vivo. RNA from isolated resistant tumor cells was obtained using Qiagen RNA extraction kit. Samples were analyzed by bioanalyzer. Poly-A sequencing was selected for library preparation, and samples were sequenced using Illumina Hi-Seq 2500 platform with 1x50 bp settings in the Centre of Genomic Regulation (CRG). Quality raw data was performed with FastQC software. Raw reads were then aligned with the STAR mapper to the Mus musculus genome and raw counts of reads per gene was additionally obtained with STAR. Differentially expression was assessed using DESeq2 version 1.30.1 package from R/Bioconductor. Among all the results, we have seen that those IRT cells have a downregulation of the antigen presentation machinery (APM) and an enrichment of stemness signatures. Overall, the results support the notion that ICB resistance emerge from low APM activity cell populations with associated stem cell-like phenotype.

2022-01-04 | GSE176580 | GEO

Preclinical model of anti-PDL1 Immune-checkpoint blockade (ICB) resistance in breast cancer associated to low antigen presentation machinery (APM)

Project description:Preclinical model of anti-PDL1 Immune-checkpoint blockade (ICB) resistance in breast cancer associated to low antigen presentation machinery (APM)

| PRJNA736735 | ENA

Microbial mechanisms to improve immune checkpoint blockade responsiveness.

Project description: Not available

| S-EPMC9284443 | biostudies-literature

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

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 bulk RNA-seq, single-cell RNA-seq and single-cell ATAC-seq.

2022-11-29 | GSE152618 | GEO

Oligomeric human Aβ1-42 inhibits antigen presentation

Project description:Oligomeric human Aβ1-42 inhibits antigen presentation

| PRJNA563674 | ENA

Increased antigen cross-presentation but impaired cross-priming after activation of PPARÎ³

Project description:Increased antigen cross-presentation but impaired cross-priming after activation of PPARÎ³ is mediated by up-regulation of B7H1 Dendritic cells (DCs) are able to take up exogenous antigens and present antigen-derived peptides on MHC class I molecules, a process termed cross-presentation. The mannose receptor (MR), an endocytic receptor expressed on a variety of antigen-presenting cells (APCs), has been demonstrated to target soluble antigens exclusively towards cross-presentation. In this study, we investigated the role of the murine nuclear receptor peroxisome proliferator-activated receptor Î³ (PPARÎ³), a ligand-activated transcription factor with immunomodulatory properties, in MR-mediated endocytosis and cross-presentation of the model antigen ovalbumin (OVA). We could demonstrate both in vitro and in vivo that activation of PPARÎ³ resulted in increased MR expression, which in consequence led to enhanced MR-mediated endocytosis and elevated cross-presentation of soluble OVA. Concomitantly, activation of PPARÎ³ in DCs induced up-regulation of the co-inhibitory molecule B7H1, which, despite enhanced cross-presentation, caused an impaired activation of naive OVA-specific CD8+ T cells and the induction of T cell tolerance. These data provide a mechanistic basis for the immunomodulatory action of PPARÎ³ which might open new possibilities in development of therapeutical approaches aimed at the control of excessive immune responses, e.g. in T cell-mediated autoimmunity. Comparison of murine mannose receptor negative versus mannose receptor positive bone marrow-derived DCs

2010-05-08 | E-GEOD-15616 | biostudies-arrayexpress

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