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YH29407 with anti-PD-1 ameliorates anti-tumor effects via increased T cell functionality and antigen presenting machinery in the tumor microenvironment

ABSTRACT: YH29407 with anti-PD-1 ameliorates anti-tumor effects via increased T cell functionality and antigen presenting machinery in the tumor microenvironment

PROVIDER: PRJNA898981 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22213737_1.fastq.gz	Fastqsanger.gz
	SRR22213737_2.fastq.gz	Fastqsanger.gz
	SRR22213738_1.fastq.gz	Fastqsanger.gz
	SRR22213738_2.fastq.gz	Fastqsanger.gz
	SRR22213739_1.fastq.gz	Fastqsanger.gz

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YH29407 with anti-PD-1 ameliorates anti-tumor effects via increased T cell functionality and antigen presenting machinery in the tumor microenvironment

Project description:Among cancer cells, indoleamine 2,3-dioxygenase1 (IDO1) activity has been implicated in improving the proliferation and growth of cancer cells and suppressing immune cell activity. IDO1 is also responsible for the catabolism of tryptophan to kynurenine. Depletion of tryptophan and an increase in kynurenine exert important immunosuppressive functions by activating regulatory T cells and suppressing CD8+ T and natural killer (NK) cells. In this study, we compared the anti-tumor effects of YH29407, the best-in-class IDO1 inhibitor with improved pharmacodynamics and pharmacokinetics, with first and second-generation IDO1 inhibitors (epacadostat and BMS-986205, respectively). YH29407 treatment alone and anti-PD-1 (aPD-1) combination treatment induced significant tumor suppression compared with competing drugs. In particular, combination treatment showed the best anti-tumor effects, with most tumors reduced and complete responses. Our observations suggest that improved anti-tumor effects were caused by an increase in T cell infiltration and activity after YH29407 treatment. Notably, an immune depletion assay confirmed that YH29407 is closely related to CD8+ T cells. RNA-seq results showed that treatment with YH29407 increased the expression of genes involved in T cell function and antigen presentation in tumors expressing ZAP70, LCK, NFACT2, B2M, and MYD88 genes. Our results suggest that an IDO1 inhibitor, YH29407, has enhanced PK/PD compared to previous IDO1 inhibitors by causing a change in the population of CD8+ T cells including infiltrating T cells into the tumor. Ultimately, YH29407 overcame the limitations of the competing drugs and displayed potential as an immunotherapy strategy in combination with aPD-1

2023-11-06 | GSE217419 | GEO

YH29407 with anti-PD-1 ameliorates anti-tumor effects <i>via</i> increased T cell functionality and antigen presenting machinery in the tumor microenvironment.

Project description:Among cancer cells, indoleamine 2, 3-dioxygenase1 (IDO1) activity has been implicated in improving the proliferation and growth of cancer cells and suppressing immune cell activity. IDO1 is also responsible for the catabolism of tryptophan to kynurenine. Depletion of tryptophan and an increase in kynurenine exert important immunosuppressive functions by activating regulatory T cells and suppressing CD8+ T and natural killer (NK) cells. In this study, we compared the anti-tumor effects of YH29407, the best-in-class IDO1 inhibitor with improved pharmacodynamics and pharmacokinetics, with first and second-generation IDO1 inhibitors (epacadostat and BMS-986205, respectively). YH29407 treatment alone and anti-PD-1 (aPD-1) combination treatment induced significant tumor suppression compared with competing drugs. In particular, combination treatment showed the best anti-tumor effects, with most tumors reduced and complete responses. Our observations suggest that improved anti-tumor effects were caused by an increase in T cell infiltration and activity after YH29407 treatment. Notably, an immune depletion assay confirmed that YH29407 is closely related to CD8+ T cells. RNA-seq results showed that treatment with YH29407 increased the expression of genes involved in T cell function and antigen presentation in tumors expressing ZAP70, LCK, NFATC2, B2M, and MYD88 genes. Our results suggest that an IDO1 inhibitor, YH29407, has enhanced PK/PD compared to previous IDO1 inhibitors by causing a change in the population of CD8+ T cells including infiltrating T cells into the tumor. Ultimately, YH29407 overcame the limitations of the competing drugs and displayed potential as an immunotherapy strategy in combination with aPD-1.

| S-EPMC9761775 | biostudies-literature

FcγR engagement reprograms neutrophils into antigen cross-presenting cells that elicit acquired anti-tumor immunity

Project description:FcγR engagement reprograms neutrophils into antigen cross-presenting cells that elicit acquired anti-tumor immunity

| PRJNA726185 | ENA

ILC2s directly activate anti-tumor cytotoxic CD8+ T lymphocytes by internalizing, processing, and presenting exogenous antigens

Project description:Type-2 innate-lymphoid cells (ILC2s) associate with both tumor promotion and inhibition. We found that ILC2s may induce anti-tumor immunity by a hitherto-unrealized mechanism: they may internalize, process, and present exogenous tumor antigen on major-histocompatibility-complex class-I (MHCI) molecules with costimulatory molecules to CD8+ T cells. This converts the T cells into cytotoxic-T-lymphocytes (CTLs). Specifically, transferring ILC2s into tumor-bearing mice inhibited tumor growth in a CD8+ T cell-dependent manner. Moreover, co-culturing human or murine CD8+ T cells with ILC2s upregulated T-cell expression of cytotoxic molecules. The resulting CTLs efficiently killed tumor cells in vitro and upon transfer into tumor-bearing mice. ILC2s were found to internalize exogenous antigens via clathrin-dependent endocytosis and to process/present them as efficiently as professional antigen-presenting cells for CD8+ T cells (type-1 conventional dendritic cells). Thus, ILC2s can present antigen to CD8+ T cells and induce their tumor-killing activity. This novel finding has promising implications for anti-tumor strategies.

2024-08-31 | GSE241945 | GEO

Epigenetic regulations in the IFNM-NM-3 signalling pathway: IFNM-NM-3-mediated MHC class I upregulation on tumour cells is associated with DNA demethylation of antigen-presenting machinery genes [TC1A9_IFN]

Project description:Reversible MHC class I deficiency on tumour cells is commonly caused by coordinated silencing of antigen-presenting machinery genes and restorable by IFNM-NM-3. Here we describe association of DNA demethylation of selected antigen-presenting machinery gene regulatory regions located in the MHC genomic locus (TAP-1, TAP-2, LMP-2, LMP-7) upon IFNM-NM-3 treatment with MHC class I upregulation on tumour cells. Our novel findings demonstrate that IFNM-NM-3 acts as an epigenetic modifier upregulating the expression of antigen-presenting machinery genes through DNA demethylation. Our data also cast more light on the role of DNA methylation in tumour cell escape from specific immunity. TC-1/A9 cultured cells treated with IFN gama or nothing. 3 biological replicates per condition.

2014-12-08 | E-GEOD-53467 | biostudies-arrayexpress

Project description:Reversible MHC class I deficiency on tumour cells is commonly caused by coordinated silencing of antigen-presenting machinery genes and restorable by IFNM-NM-3. Here we describe association of DNA demethylation of selected antigen-presenting machinery gene regulatory regions located in the MHC genomic locus (TAP-1, TAP-2, LMP-2, LMP-7) upon IFNM-NM-3 treatment with MHC class I upregulation on tumour cells. Our novel findings demonstrate that IFNM-NM-3 acts as an epigenetic modifier upregulating the expression of antigen-presenting machinery genes through DNA demethylation. Our data also cast more light on the role of DNA methylation in tumour cell escape from specific immunity. TC-1/A9 cultured cells treated with DAC/TSA or nothing. 3 biological replicates per condition.

2014-12-08 | E-GEOD-53466 | biostudies-arrayexpress

Project description:Reversible MHC class I deficiency on tumour cells is commonly caused by coordinated silencing of antigen-presenting machinery genes and restorable by IFNM-NM-3. Here we describe association of DNA demethylation of selected antigen-presenting machinery gene regulatory regions located in the MHC genomic locus (TAP-1, TAP-2, LMP-2, LMP-7) upon IFNM-NM-3 treatment with MHC class I upregulation on tumour cells. Our novel findings demonstrate that IFNM-NM-3 acts as an epigenetic modifier upregulating the expression of antigen-presenting machinery genes through DNA demethylation. Our data also cast more light on the role of DNA methylation in tumour cell escape from specific immunity. RVP3 cultured cells treated with DAC/TSA or nothing. 3 biological replicates per condition.

2014-12-08 | E-GEOD-53465 | biostudies-arrayexpress

Epigenetic regulations in the IFNγ signalling pathway: IFNγ-mediated MHC class I upregulation on tumour cells is associated with DNA demethylation of antigen-presenting machinery genes [RVPC3_DAC]

Project description:Reversible MHC class I deficiency on tumour cells is commonly caused by coordinated silencing of antigen-presenting machinery genes and restorable by IFNγ. Here we describe association of DNA demethylation of selected antigen-presenting machinery gene regulatory regions located in the MHC genomic locus (TAP-1, TAP-2, LMP-2, LMP-7) upon IFNγ treatment with MHC class I upregulation on tumour cells. Our novel findings demonstrate that IFNγ acts as an epigenetic modifier upregulating the expression of antigen-presenting machinery genes through DNA demethylation. Our data also cast more light on the role of DNA methylation in tumour cell escape from specific immunity.

2014-12-08 | GSE53465 | GEO

Epigenetic regulations in the IFNγ signalling pathway: IFNγ-mediated MHC class I upregulation on tumour cells is associated with DNA demethylation of antigen-presenting machinery genes [TC1A9_IFN]

Project description:Reversible MHC class I deficiency on tumour cells is commonly caused by coordinated silencing of antigen-presenting machinery genes and restorable by IFNγ. Here we describe association of DNA demethylation of selected antigen-presenting machinery gene regulatory regions located in the MHC genomic locus (TAP-1, TAP-2, LMP-2, LMP-7) upon IFNγ treatment with MHC class I upregulation on tumour cells. Our novel findings demonstrate that IFNγ acts as an epigenetic modifier upregulating the expression of antigen-presenting machinery genes through DNA demethylation. Our data also cast more light on the role of DNA methylation in tumour cell escape from specific immunity.

2014-12-08 | GSE53467 | GEO

Epigenetic regulations in the IFNγ signalling pathway: IFNγ-mediated MHC class I upregulation on tumour cells is associated with DNA demethylation of antigen-presenting machinery genes [TC1A9_DAC]

Project description:Reversible MHC class I deficiency on tumour cells is commonly caused by coordinated silencing of antigen-presenting machinery genes and restorable by IFNγ. Here we describe association of DNA demethylation of selected antigen-presenting machinery gene regulatory regions located in the MHC genomic locus (TAP-1, TAP-2, LMP-2, LMP-7) upon IFNγ treatment with MHC class I upregulation on tumour cells. Our novel findings demonstrate that IFNγ acts as an epigenetic modifier upregulating the expression of antigen-presenting machinery genes through DNA demethylation. Our data also cast more light on the role of DNA methylation in tumour cell escape from specific immunity.

2014-12-08 | GSE53466 | GEO

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