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TOX is a critical regulator of tumour-specific T cell differentiation

ABSTRACT: TOX is a critical regulator of tumour-specific T cell differentiation

PROVIDER: PRJNA523935 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8614900_1.fastq.gz	Fastqsanger.gz
	SRR8614900_2.fastq.gz	Fastqsanger.gz
	SRR8614920_1.fastq.gz	Fastqsanger.gz
	SRR8614920_2.fastq.gz	Fastqsanger.gz
	SRR8614930_1.fastq.gz	Fastqsanger.gz

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TOX is a critical regulator of tumour-specific T cell differentiation.

Project description:Tumour-specific CD8 T cell dysfunction is a differentiation state that is distinct from the functional effector or memory T cell states1-6. Here we identify the nuclear factor TOX as a crucial regulator of the differentiation of tumour-specific T (TST) cells. We show that TOX is highly expressed in dysfunctional TST cells from tumours and in exhausted T cells during chronic viral infection. Expression of TOX is driven by chronic T cell receptor stimulation and NFAT activation. Ectopic expression of TOX in effector T cells in vitro induced a transcriptional program associated with T cell exhaustion. Conversely, deletion of Tox in TST cells in tumours abrogated the exhaustion program: Tox-deleted TST cells did not upregulate genes for inhibitory receptors (such as Pdcd1, Entpd1, Havcr2, Cd244 and Tigit), the chromatin of which remained largely inaccessible, and retained high expression of transcription factors such as TCF-1. Despite their normal, 'non-exhausted' immunophenotype, Tox-deleted TST cells remained dysfunctional, which suggests that the regulation of expression of inhibitory receptors is uncoupled from the loss of effector function. Notably, although Tox-deleted CD8 T cells differentiated normally to effector and memory states in response to acute infection, Tox-deleted TST cells failed to persist in tumours. We hypothesize that the TOX-induced exhaustion program serves to prevent the overstimulation of T cells and activation-induced cell death in settings of chronic antigen stimulation such as cancer.

| S-EPMC7698992 | biostudies-literature

TOX is a critical regulator of tumour-specific T cell differentiation

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-06-24 | GSE126974 | GEO

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

Kaiso, a critical regulator of spermatogenesis

Project description:Kaiso, a critical regulator of spermatogenesis

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Bach2 is a critical negative regulator of Tfh cell differentiation

Project description:Bach2 is a critical negative regulator of Tfh cell differentiation

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

Project description:TOX is selectively expressed in tumor-infiltrating CD8 T cells however the role of TOX in peripheral CD8 T cells is not known. The two goals of this study are to elucidate transcriptional changes between TOX-sufficient and TOX-deficient tumor infiltrating CD8 T cells and to elucidate the molecular program induced by TOX overexpression in peripheral CD8 T cells.

2019-06-24 | GSE126973 | GEO

Innate lymphoid cell development requires TOX-dependent generation of a common ILC progenitor

Project description:Subtypes of innate lymphoid cells (ILC), defined by effector function and transcription factor expression, have recently been identified. In the adult, ILC derive from common lymphoid progenitors in bone marrow, although transcriptional regulation of the developmental pathways involved remains poorly defined. TOX is required for development of lymphoid tissue inducer cells, a type of ILC3 required for lymph node organogenesis, and NK cells, a type of ILC1. We show here that production of multiple ILC lineages requires TOX, as a result of TOX-dependent development of common ILC progenitors. Comparative transcriptome analysis demonstrated failure to induce various aspects of the ILC gene program in the absence of TOX, implicating this nuclear factor as a key early determinant of ILC lineage specification. TOX KO vs. wild tyype

2015-04-27 | E-GEOD-65850 | biostudies-arrayexpress

ATACseq profiling of various TOX+ and TOX- tumor-infiltrating CD8 T cells

Project description:TOX is selectively expressed in tumor-infiltrating CD8 T cells however the role of TOX in peripheral CD8 T cells is not known. The goal of this study is to elucidate changes in chromatin accessibility determined by ATAC-seq between TOX-sufficient and TOX-deficient tumor infiltrating CD8 T cells isolated from murine tumors.

2019-06-24 | GSE126970 | GEO

Oncogenic role of TOX in CTCL

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Myokine irisin is a critical regulator of cognitive function

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