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TET2 promotes anti-tumor immunity by governing G-MDSCs and CD8+ T cell numbers

ABSTRACT: TET2 promotes anti-tumor immunity by governing G-MDSCs and CD8+ T cell numbers

PROVIDER: PRJNA604913 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11024636_1.fastq.gz	Fastqsanger.gz
	SRR11024636_2.fastq.gz	Fastqsanger.gz
	SRR11024637_1.fastq.gz	Fastqsanger.gz
	SRR11024637_2.fastq.gz	Fastqsanger.gz
	SRR11024638_1.fastq.gz	Fastqsanger.gz

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TET2 promotes anti-tumor immunity by governing G-MDSCs and CD8+ T cell numbers

Project description:Host immune response is a fundamental mechanism for attenuating cancer progression. Here we report a pivotal role of the DNA demethylase and tumor suppressor TET2 played in host antitumor immunity. Deletion of Tet2 dramatically elevated the IL-6 level in Tet2-/- mice upon tumor challenge. The elevated IL-6 greatly stimulated the immunosuppressive granulocytic myeloid-derived suppressor cells (G-MDSCs), which in turn significantly reduced CD8+ T cells upon tumor challenge. Consequently, systematic knockout of the Tet2 in mice led to accelerated syngeneic tumor growth, which was constrained by anti-PD-1 blockade. Removal of G-MDSCs by the anti-mouse Ly6g Ab restored the numbers of CD8+ T cells in Tet2-/- mice and rebooted their anti-tumor activity. Importantly, anti-IL-6 Ab treatment blocked the expansion of G-MDSCs and inhibited syngeneic tumor growth. Collectively, these findings reveal a TET2-mediated IL-6/G-MDSC/CD8+ T immune response cascade that safeguards host adaptive anti-tumor immunity, offering a cell non-autonomous mechanism of TET2 for tumor suppression.

2020-08-04 | GSE144787 | GEO

TET2 promotes anti-tumor immunity by governing G-MDSCs and CD8<sup>+</sup> T-cell numbers.

Project description:The host immune response is a fundamental mechanism for attenuating cancer progression. Here we report a role for the DNA demethylase and tumor suppressor TET2 in host anti-tumor immunity. Deletion of Tet2 in mice elevates IL-6 levels upon tumor challenge. Elevated IL-6 stimulates immunosuppressive granulocytic myeloid-derived suppressor cells (G-MDSCs), which in turn reduce CD8+ T cells upon tumor challenge. Consequently, systematic knockout of Tet2 in mice leads to accelerated syngeneic tumor growth, which is constrained by anti-PD-1 blockade. Removal of G-MDSCs by the anti-mouse Ly6g antibodies restores CD8+ T-cell numbers in Tet2-/- mice and reboots their anti-tumor activity. Importantly, anti-IL-6 antibody treatment blocks the expansion of G-MDSCs and inhibits syngeneic tumor growth. Collectively, these findings reveal a TET2-mediated IL-6/G-MDSCs/CD8+ T-cell immune response cascade that safeguards host adaptive anti-tumor immunity, offering a cell non-autonomous mechanism of TET2 for tumor suppression.

| S-EPMC7534639 | biostudies-literature

Expression data from MDSCs at different time points during tumor progression

Project description:Myeloid-derived suppressor cells (MDSCs) are increased by tumor-derived factors and suppress anti-tumor immunity. MDSCs obtained at a late time point after tumor injection had stronger suppressive activity than MDSCs obtained at an early time point, as measured by T cell proliferation assays. To find factors in MDSCs that change during tumor growth, we analyzed gene expression profiles from MDSCs at different time points after tumor injection. We found that immune response-related genes were down-regulated, but pro-tumor function-related genes were up-regulated in both Mo-MDSCs and PMN-MDSCs at the late time point. Among differentially expressed genes, FK506 binding protein 51 (FKBP51), which is a member of the immunophilin protein family and plays a role in immunoregulation, was increased in the Mo- and PMN-MDSCs isolated from the late time points. Experiments using siRNA and a chemical inhibitor of FKBP51 revealed that FKBP51 contributes to the regulation of the suppressive function of MDSCs by increasing iNOS, ARG1, and ROS levels and enhancing NF-kappaB activity. Collectively, our data suggest that FKBP51 is a novel molecule that can be targeted to regulate the immunosuppressive function of MDSCs. To identify the factors that licensed MDSCs to be more suppressive as tumors grow, we analyzed gene expression profiles in the two subsets of MDSCs at different time points (3wks, 6wks) during tumor progression. CD11b+Ly-6C(high)Ly-6G(low) Mo-MDSCs and CD11b+Ly-6C(low)Ly-6G(high) PMN-MDSCs were sorted from pooled spleens of naÃ¯ve mice and Her-2/CT26 tumor-bearing mice. Total RNA was purified and gene expression was analyzed by the Affymetrix GeneChipÂ® Mouse Gene 1.0 ST Array.

2012-03-29 | E-GEOD-35398 | biostudies-arrayexpress

TET2-mediated mRNA in tumor immunity [m5C]

Project description:TET2-mediated mRNA in tumor immunity [m5C]

| PRJNA963841 | ENA

TET2 deficiency subverts tumor immunity [model 3]

Project description:TET2 deficiency subverts tumor immunity [model 3]

| PRJNA851067 | ENA

Label free quantitativeproteomics of MDSCs

Project description:We sorted the MDSCs from the bone marrows of B16-F10 tumor-bearing mice and the naive mice. In addition, we cultured MDSCs in vitro to determine the effect of DOX (5µM).

2022-02-17 | PXD027863 | Pride

TET2 deficiency subverts tumor immunity [model 3]

Project description:To investigate the function of TET2 in the development of acute myeloid leukemia (AML), we performed gene expression profiling analysis using data obtained from RNA-seq of AML cells carrying Tet2+/+ versus Tet2-/-.

2023-06-23 | GSE206487 | GEO

Expression data from MDSCs at different time points during tumor progression

2012-03-30 | GSE35398 | GEO

TET2-mediated mRNA in tumor immunity [m5C]

Project description:To investigate the function of TET2 as an mRNA m5C demethylase in the development of acute myeloid leukemia (AML), we conducted RNA bisulfite sequencing of mRNA samples enriched from AML cells carrying Tet2+/+ versus Tet2-/- with actinomycin D treatment at different time point.

2023-06-23 | GSE231329 | GEO

RNA sequencing of in vivo sorted C12FDG+ MDSCs and C12FDG- MDSCs

Project description:RNA sequencing of in vivo sorted C12FDG+ MDSCs and C12FDG- MDSCs

2023-03-02 | GSE200077 | GEO