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Anti-CD137 drives early epigenetic remodeling of Tex cell associated genes

ABSTRACT: Anti-CD137 drives early epigenetic remodeling of Tex cell associated genes

PROVIDER: PRJNA949175 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23979300_1.fastq.gz	Fastqsanger.gz
	SRR23979300_2.fastq.gz	Fastqsanger.gz
	SRR23979301_1.fastq.gz	Fastqsanger.gz
	SRR23979301_2.fastq.gz	Fastqsanger.gz
	SRR23979302_1.fastq.gz	Fastqsanger.gz

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Anti-CD137 drives early epigenetic remodeling of Tex cell associated genes

Project description:To understand the mechanism of CD137 induced exhaustion program, we analyzed the splenic CD44hi CD8+ T cell chromatin states along anti-CD137 treatment through assay for transposase-accessible chromatin using sequencing (ATAC-seq)

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Transcriptomic analysis of VK12653 Multiple Myeloma bone marrow microenvironmentupon treatment with anti-CD137 agonists

Project description:We report the RNA sequencing of VK12653 Multiple Myeloma bone marrow microenvironment upon treatment with anti-CD137 agonists

2023-06-30 | GSE206545 | GEO

CD137 (4-1BB) requires physically associated cIAPs for signal transduction and antitumor effects

Project description:CD137 (4-1BB) is a member of the TNFR family that mediates potent T-cell costimulatory signals upon ligation by CD137L or agonist monoclonal antibodies. CD137 agonists attain immunotherapeutic antitumor effects in cancer mouse models and multiple agents of this kind are undergoing clinical trials. We show that cIAP1 and cIAP2 are physically associated with the CD137-signaling complex. Moreover, cIAPs are required for CD137 signaling towards the NF-κB and MAPK pathways and for costimulation of human and mouse T lymphocytes. Functional evidence was substantiated with SMAC-mimetics that trigger cIAPs degradation and by transfecting cIAP dominant-negative variants. Antitumor effects of agonist anti-CD137 mAbs are critically dependent on the integrity of cIAPs in cancer mouse models and cIAPs are also required for signaling from CARs encompassing CD137’s cytoplasmic tail.

2024-05-24 | PXD042585 | Pride

An agonistic anti-CD137 antibody promotes inflammatory signatures in immune cells that disrupt germinal center formation and T cell-dependent antibody responses

Project description:CD137 is a costimulatory receptor expressed on natural killer cells, T cells, and subsets of dendritic cells. An agonistic monoclonal antibody (mAb) against CD137 has been used to reduce tumor burden or reverse autoimmunity in animal models and clinical trials. When testing the ability of agonistic anti-CD137 mAb to promote clearance of persistent virus infection, we recently reported reduced numbers of germinal center B (GC B) cells and follicular dendritic cells (FDC) in lymphoid tissues. Here, we show that agonistic anti-CD137 agonistic mAb treatment impairs antibody responses with multiple T cell-dependent antigens including virus infection, recombinant viral antigens, and conjugated haptens but not with a T cell-independent antigen or at homeostasis. These effects were not due to enhanced apoptosis or impaired proliferation of B cells but instead correlated with disorganization of the stromal cell compartment of the GC, and were mediated by CD137 signaling in CD4+ and CD8+ T cells. Anti-CD137 treatment in the context of acute infection also resulted in reduced numbers of marginal zone B cells, greater numbers of antibody-secreting plasmablasts, and pro-inflammatory signatures in several myeloid and lymphoid cell populations of the spleen. Our experiments in mice suggest that agonistic anti-CD137 mAbs used in cancer and autoimmunity therapy may alter stromal cell populations to causes GC collapse and impaired long-term antibody and B cell memory responses.

2019-12-31 | GSE141111 | GEO

An agonistic anti-CD137 antibody promotes inflammatory signatures in immune cells that disrupt germinal center formation and T cell-dependent antibody responses II

2019-12-31 | GSE141117 | GEO

CD137 costimulation counteracts TGFβ inhibition of NK cell anti-tumor function and promotes the acquisition of tissue-resident Th9-like properties [4 treatments]

Project description:Enhancing NK cell-based cancer immunotherapy by overcoming immunosuppression is an unmet goal. Here, we demonstrate the ability of the anti-CD137 agonist urelumab for overcoming TGF-β-mediated inhibition of human NK-cell proliferation and sustained anti-tumor function. Transcriptomic, immunophenotypic and functional analyses evidenced that CD137 costimulation modified the transcriptional program induced by TGF-β on activated NK cells by limiting SMAD4-dependent inhibition of pro-proliferative (CD25, cMyc), activating (NKG2D, CD16) and effector (Granzyme B, IFNγ) molecules while maintaining SMAD4-independent acquisition of tumor-retention features (CXCR3, CD103). Activated NK cells cultured in the presence of TGF-β1 and CD137 agonist showed preserved antibody-dependent cytotoxicity against cancer cells, recovered CCL5 and IFNγ secretion and gained the capacity for producing IL-9 upon restimulation. Treatment of breast tumor-derived multicellular cultures with trastuzumab and urelumab recapitulated CD137 induction and fostered tumor-infiltrating CD16+ NK cell persistence. Our data reveals CD137 as a targetable checkpoint for overturning TGF-β constrains on NK cell anti-tumor responses.

2021-09-10 | GSE143375 | GEO

CD137 costimulation counteracts TGFβ inhibition of NK cell anti-tumor function and promotes the acquisition of tissue-resident Th9-like properties [2 treatments]

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CD137 agonism enhances anti-PD1 induced activation of clonally expanded CD8+ T cells in a neoadjuvant pancreatic cancer clinical trial

Project description:Successful pancreatic ductal adenocarcinoma (PDAC) immunotherapy requires therapeutic combinations that induce quality T cells. Tumor microenvironment (TME) analysis following therapeutic interventions can identify response mechanisms to guide design of more effective combinations. We provide a reference single-cell dataset from PDAC-infiltrating T cell and monocyte subsets from a human neoadjuvant clinical trial comparing the granulocyte-macrophage colony-stimulating factor (GM-CSF)-secreting allogeneic PDAC vaccine GVAX alone, in combination with anti-PD1, or with both anti-PD1 and a CD137 agonist. Tumor infiltrating leukocytes analyzed two weeks post neoadjuvant therapy revealed shifts in CD8+ T cell activation as well as cytoskeletal and extracellular matrix (ECM)-interacting components with Cy/GVAX and anti-PD1. Addition of a CD137 agonist was associated with increased abundance of activated and clonally expanded CD8+ T cells with distinct perturbations in cytoskeletal and ECM components. Furthermore, a new computational method to compare ligand-receptor networks between patients from different treatment arms found that CD137 agonism is associated with immunosuppressive TREM2 signaling in tumor associated macrophages (TAMs) that corresponds to changes in cell metabolism, function, and ECM interactions. Altogether these findings associate therapy with GVAX, anti-PD1, and CD137 agonist with enhanced CD8+ T cell function while inducing alternative immunosuppressive pathways in patients with PDAC.

2024-12-16 | GSE279781 | GEO

Single cell Transcriptomic analysis of CD8+ T cells treated with anti-CD137 agonists within VK12653 Multiple Myeloma bone marrow microenvironment .

Project description:We report the single cell RNA sequencing of mouse CD8+ T cells infiltrating VK12653 Multiple Myeloma lesions upon treatment with anti-CD137 agonists .

2023-06-30 | GSE205702 | GEO

CD137-CIS IO

Project description:CD137 cis-costimulation is superior to trans-costimulation at inducing transcriptomic differences in T-cell proliferation and DNA repair programs We used microarrays to detail differentially expressed genes of cis- and trans CD137-costimulated CD8 T cells with respect to CD3-TCR stimulation

2021-09-28 | GSE158041 | GEO

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