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Stat5 antagonizes Tox and CD8 T cell exhaustion to foster a durable effector-like state during chronic antigen exposure

ABSTRACT: Stat5 antagonizes Tox and CD8 T cell exhaustion to foster a durable effector-like state during chronic antigen exposure

PROVIDER: PRJNA998411 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25423025_1.fastq.gz	Fastqsanger.gz
	SRR25423025_2.fastq.gz	Fastqsanger.gz
	SRR25423026_1.fastq.gz	Fastqsanger.gz
	SRR25423026_2.fastq.gz	Fastqsanger.gz
	SRR25423027_1.fastq.gz	Fastqsanger.gz

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Stat5 antagonizes Tox and CD8 T cell exhaustion to foster a durable effector-like state during chronic antigen exposure

Project description:Constitutive Stat5a activity antagonized Tox and rewired CD8 T cells away from exhaustion to acquire a durable effector/NK-like state with superior anti-tumor potential Stat5 fostered TEXint, temporally re-engaging the Stat5 pathway, partially reprogrammed the epigenetic landscape of exhaustion and restored effector-like differentiation and function cell formation and partial re-acquisition of effector-biology during this TEXprog-to-TEXint transition,

2023-08-31 | GSE238239 | GEO

Enhanced STAT5a activation opposes Tox and rewires exhausted CD8 T cells towards a hybrid durable effector-like state during chronic stimulation [CITE-seq_PostInfection]

2023-05-31 | GSE214114 | GEO

Enhanced STAT5a activation opposes Tox and rewires exhausted CD8 T cells towards a hybrid durable effector-like state during chronic stimulation [scRNA-seq_PostInfection]

2023-05-31 | GSE214113 | GEO

Enhanced STAT5a activation opposes Tox and rewires exhausted CD8 T cells towards a hybrid durable effector-like state during chronic stimulation [ATAC-Seq]

Project description:Here, we discovered a reciprocal antagonism between Stat5a and Tox in TEX cells. Stat5a antagonized the Tox-mediated exhaustion program to achieve a durable and protective hybrid effector/NK-like differentiation state in settings that typically drive exhaustion. Stat5 also drove TEX progenitors to differentiate into the effector-like TEXint subset, a key developmental step for PD-1 blockade responsiveness. Therapeutic enhancement of Stat5 activity in TEX cells using an orthogonal IL-2/IL2Rb pair system fostered TEXint cell accumulation and synergized with PD-L1 blockade. Finally, targeted delivery of Stat5-signals in TEX progenitors achieved partial epigenetic rewiring of these cells towards the effector/memory lineage and revived polyfunctionality. Together, these data highlight therapeutic opportunities of targeting Stat5 to antagonize the Tox-dependent epigenetic programming of TEX and provoke a hybrid program that exploits effector biology and durability for optimal therapeutic potential

2023-08-31 | GSE240431 | GEO

Enhanced STAT5a activation opposes Tox and rewires exhausted CD8 T cells towards a hybrid durable effector-like state during chronic stimulation [ATAC-postChallenge]

2023-05-31 | GSE214112 | GEO

Enhanced STAT5a activation opposes Tox and rewires exhausted CD8 T cells towards a hybrid durable effector-like state during chronic stimulation [ATAC-postInfection]

2023-05-31 | GSE214111 | 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

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

STAT5 antagonism of B cell enhancer networks drives leukemia and poor patient surviva

Project description:The transcription factor STAT5 plays a critical role in B cell Acute Lymphoblastic Leukemia (B-ALL). How STAT5 mediates this effect is unclear. Here we demonstrate that STAT5 activation cooperates with defects in the pre-BCR signaling components Blnk, Btk, Prkcb, Nfkb1, and Ikzf1 to initiate B-ALL. STAT5 antagonizes NFkB and IKAROS by opposing regulation of shared target genes. STAT5 binding was enriched at super-enhancers, which were associated with an opposing network of transcription factors, including PAX5, EBF1, PU.1, IRF4, and IKAROS. Patients with high ratios of active STAT5 to NFκB or IKAROS have more aggressive disease. Our studies illustrate that an imbalance of two opposing transcriptional programs drive B-ALL, and suggest that restoring the balance of these pathways may inhibit B-ALL.

2017-04-03 | GSE86878 | 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

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