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LAG-3 sustains TOX and regulates the CD94/NKG2-Qa-1b axis to govern exhausted CD8 T cell NK receptor expression and cytotoxicity

ABSTRACT: LAG-3 sustains TOX and regulates the CD94/NKG2-Qa-1b axis to govern exhausted CD8 T cell NK receptor expression and cytotoxicity

PROVIDER: PRJNA1130418 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29664251.fastq.gz	Fastqsanger.gz
	SRR29664252.fastq.gz	Fastqsanger.gz
	SRR29664253.fastq.gz	Fastqsanger.gz
	SRR29664254.fastq.gz	Fastqsanger.gz
	SRR29664255.fastq.gz	Fastqsanger.gz

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Similar Datasets

LAG-3 sustains TOX and regulates the CD94/NKG2-Qa-1b axis to govern exhausted CD8 T cell NK receptor expression and cytotoxicity

Project description:Exhausted CD8 T cells (Tex) found in chronic viral infection and cancer are defined by sustained co-expression of inhibitory receptors (IRs). Tex can be reinvigorated by blocking IRs, such as PD-1, but synergistic reinvigoration of Tex and enhanced disease control can be achieved by co-targeting multiple IRs including co-blockade of PD-1 and LAG-3, a treatment recently FDA-approved for melanoma. Despite the promise of anti-PD-1/anti-LAG-3 therapy, the cellular and molecular changes intrinsic to CD8 T cells when one or more of these IR pathways are disrupted remain poorly understood. To dissect these IR pathways and their interactions with each other, we used a quadruple co-transfer model to investigate the impact of singular or combined loss of PD-1 and LAG-3 on the differentiation of Tex during chronic viral infection. These analyses revealed distinct roles of PD-1 and LAG-3 in regulating Tex proliferation and cytokine/cytotoxic functions, respectively. Moreover, these studies identified key roles for LAG-3 that complement PD-1 biology including an essential role for LAG-3 in sustaining TOX expression and associated Tex durability. Finally, these studies uncovered a LAG-3-dependent circuit for the generation of an effector-like CD94/NKG2+ subset of Tex capable of enhanced cytotoxicity mediated by recognition of the stress-induced ligand Qa-1b with similar regulation of CD94/NKG2 family members in humans with combination anti-PD-1/anti-LAG-3. These analyses identify a role for LAG-3 in governing CD8 T cell Qa-1b-restricted immune sensing and surveillance. Together, these results disentangled the underlying non-redundant mechanisms of PD-1 and LAG-3 and their synergy in regulating Tex revealing additional immunotherapeutic opportunities based on these pathways.

2025-03-01 | GSE271184 | GEO

CD94-CD56dim, CD94+CD56dim and CD94+CD56hi natural killer (NK) cell comparison

Project description:CD94-CD56dim, CD94+CD56dim and CD94+CD56hi natural killer (NK) cell comparison

| PRJNA504633 | ENA

CD94-CD56dim, CD94+CD56dim and CD94+CD56hi natural killer (NK) cell chromatin histone modification assay

Project description:CUT and RUN was performed for 3 NK populations and found CD94+CD56hi NK cells exhibit unique H3K4me1, H3K4me4 enriched region, we also identified TCF7 binding region in CD94+CD56hi NK cells.

2019-12-10 | GSE122549 | GEO

CD94-CD56dim, CD94+CD56dim and CD94+CD56hi natural killer (NK) cell comparison

Project description:We compared transcriptomes of 3 NK populations and found CD94+CD56hi NK cells exhibit unique transcriptome.

2019-12-10 | GSE122324 | GEO

CD94-CD56dim, CD94+CD56dim and CD94+CD56hi natural killer (NK) cell chromatin accessibility assay

Project description:CD94-CD56dim, CD94+CD56dim and CD94+CD56hi natural killer (NK) cell chromatin accessibility assay

| PRJNA505524 | ENA

CD94-CD56dim, CD94+CD56dim and CD94+CD56hi natural killer (NK) cell chromatin accessibility assay

Project description:ATAC-Seq was performed for 3 NK populations and found CD94+CD56hi NK cells exhibit unique chromatin accessible region

2019-12-10 | GSE122548 | GEO

CD94-CD56dim, CD94+CD56dim and CD94+CD56hi natural killer (NK) cell chromatin histone modification assay

Project description:CD94-CD56dim, CD94+CD56dim and CD94+CD56hi natural killer (NK) cell chromatin histone modification assay

| PRJNA505525 | ENA

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

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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