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IL-15 complex enhances agonistic anti-CD40 + anti-PDL1 by correcting the T-bet to Tox ratio in CD8+ T cells infiltrating pancreatic ductal adenocarcinoma

ABSTRACT: IL-15 complex enhances agonistic anti-CD40 + anti-PDL1 by correcting the T-bet to Tox ratio in CD8+ T cells infiltrating pancreatic ductal adenocarcinoma

PROVIDER: PRJNA1206921 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31899574.fastq.gz	Fastqsanger.gz
	SRR31899575.fastq.gz	Fastqsanger.gz
	SRR31899576.fastq.gz	Fastqsanger.gz
	SRR31899577.fastq.gz	Fastqsanger.gz
	SRR31899578.fastq.gz	Fastqsanger.gz

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IL-15 complex enhances agonistic anti-CD40 + anti-PDL1 by correcting the T-bet to Tox ratio in CD8+ T cells infiltrating pancreatic ductal adenocarcinoma

Project description:Single cell RNA sequencing paired with single cell V(D)J sequenction of immune cells infiltrating orthotopic KPC2a tumors, spleen cells, and CD8 T cells enriched from spleen cells on day 14 posttumor. Cohorts received no treatment, agonistic anti-CD40, anti-PD-L1 or the combination of agonistic anti-CD40 + anti-PDL1. Treatments were initated on day 7 posttumor.

2025-03-05 | GSE285902 | GEO

Transcriptomic analysis of 4NQO-induced oral squamous cell carcinoma with agonistic anti-CD40 treatment

Project description:To investigate the anti-tumor effect of agonistic anti-CD40, 4NQO-indued OSCC mice with agonistic anti-CD40.

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Oncogenic role of TOX in CTCL

Project description:TOX is a nuclear factor essential for the development of CD4+ T cells in the thymus. TOX is found to be aberrantly up-regulated in the skin biopsies and in the blood CD4+ T cells of cutaneous T cell lymphoma. The goal of this study is to identify potential transcriptional targets of TOX in CTCL by comparison between TOX shRNA transfected CTCL cells (Hut78 and HH) and control CTCL cells. Two color experiment. Lentivirus transduced control vector vs. TOX shRNA vectors on Hut78 and HH cell lines. Biological replicates: 3 control replicates, 3 shRNA tansduced replicates for each cell line.

2014-04-29 | E-GEOD-57122 | biostudies-arrayexpress

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.

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VEGF-A drives TOX-dependent T cell exhaustion in anti–PD-1–resistant microsatellite stable colorectal cancers

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

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Transcriptome analysis of various TOX+ and TOX- tumor-infiltrating CD8 T cells and in vitro TOX over-expressing T cells.

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