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A network of intra and extra-tumoural cytotoxic T cells with precursor and residency features constrained by TGF-b

ABSTRACT: A network of intra and extra-tumoural cytotoxic T cells with precursor and residency features constrained by TGF-b

PROVIDER: PRJNA1065885 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27597063_1.fastq.gz	Fastqsanger.gz
	SRR27597063_2.fastq.gz	Fastqsanger.gz
	SRR27597064_1.fastq.gz	Fastqsanger.gz
	SRR27597064_2.fastq.gz	Fastqsanger.gz
	SRR27597065_1.fastq.gz	Fastqsanger.gz

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A network of intra and extra-tumoural cytotoxic T cells with precursor and residency features constrained by TGF-b

Project description:Anti-tumour immunity is limited by loss of T cell function and sustained expression of inhibitory receptors or immune checkpoints, including PD-1, a state known as T cell exhaustion. Exhausted T cells are maintained by precursors of exhausted T (TPEX) cells, that self-renew and generate effector cells, particularly in response to therapeutic immune checkpoint blockade (ICB). Similarly, tissue-resident memory T (TRM)-like cells have been implicated in tumour control and ICB response. However, the factors governing TPEX and TRM-like cell differentiation and function within the tumour environment, their relationship, and their response to ICB, remain insufficiently understood. Using single cell RNA sequencing and innovative mouse models that enable the identification and targeting of both TPEX and TRM-like cells within and outside the tumour microenvironment, we systemically dissect the developmental and functional relationship between tumour-responsive TPEX cells in the tumour microenvironment and in lymph nodes. We show that within the tumour microenvironment, TPEX cells and their progeny could acquire a tissue residency program that limits their contribution to tumour control and response to checkpoint inhibition. In contrast, stem-like TPEX cells, dependent on the transcription factor MYB and located within the tumour-draining lymph nodes (tdLN), were essential for fueling CD8+ T cell tumour infiltration and response to ICB. We identify TGF-β as the common factor enforcing residency of TPEX cells in the tumour and limiting the abundance of stem-like TPEX cells in tdLN. Finally, we provide evidence for the presence of a similar network of intra- and extratumoural CD8+ T cells in human cancer, exhibiting precursor and residency characteristics that is constrained by TGF-β.

2025-05-27 | GSE253487 | GEO

Cohesin residency determines chromatin loop patterns

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Cohesin residency determines chromatin loop patterns

Project description:Cohesin residency determines chromatin loop patterns

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Hepatic leukemia factor directs tissue residency of proinflammatory CD4+ T cells

Project description:CD4+ tissue-resident memory T cells (TRM) contribute to both host defense and pathogenesis of chronic inflammatory diseases. However, the molecular mechanisms that direct tissue residency and functional heterogeneity of CD4+ TRM remain unknown. We herein show that the transcription factor, hepatic leukemia factor (HLF), directs the tissue residency program and functionality of CD4+ TRM. HLF simultaneously upregulates tissue retention receptors and downregulates tissue egress receptors via changes in chromatin accessibility, and drives proinflammatory CD4+ TRM by inducing Bhlhe40. Genetic deletion of Hlf inhibits CD4+ TRM generation, consequently ameliorating airway tissue inflammation in vivo. In humans, HLF-positive CD4+ TRM from inflamed airway tissue have a tissue residency signature and express inflammatory cytokines. HLF is therefore a central regulator of proinflammatory CD4+ TRM development and function.

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Hepatic leukemia factor directs tissue residency of proinflammatory CD4+ T cells [bulk]

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Runx3 drives a tissue residency program that is absent in CD4+ T cells [ATAC-seq]

Project description:Tissue-resident memory T (TRM) cells provide rapid and superior control of localized infections. The transcription factor Runx3 was recently identified as a master regulator of CD8+ T cell tissue residency. However, Runx3 also drives CD8+ T cell lineage commitment and is repressed in CD4+ T cells, raising the possibility that this transcription factor defines a form of tissue residency unique to the CD8+ T cell subset. Here, we show that as a direct consequence of Runx3-deficiency, CD4+ TRM cells in epithelia lack the TGFb-responsive transcriptional network that underpins CD8+ TRM cell residency. Ectopic Runx3 expression in CD4+ T cells rescued this transcriptional program to promote prolonged survival, decreased tissue egress and a microanatomical redistribution towards epithelial layers that combined, resulted in superior local immune protection. Our results thus reveal a mechanistic discordance between CD4+ and CD8+ TRM cell formation in barrier tissues that is controlled by Runx3. Consequently, CD4+ TRM cells are unable to adopt a type of tissue residency that is intrinsically accessible to the CD8+ TRM cell subset.

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Runx3 drives a tissue-residency program that is absent in CD4+ T cells [RNA-seq]

Project description:Pattens of tissue-residency differs between CD4+ and CD8+ memory T cells in evironmentally exposed organs. The lineage-controlling transcription factor Runx3, expressed in CD8+ T cells, is responsible for shaping a tissue-resident gene network in response to the cytokine TGF-b. While the lack of Runx3 by CD4+ T cells precludes these transcriptional changes, Runx3-overexpression in CD+ T cells enable phenotypical, transcriptional and functional changes to allow residency.

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single cell RNA sequencing of intra- and extra- articular ligaments in mice

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Gene expression profiles at single cell level of CD45+ tumor-infiltrating immune cells in intra- and extra-cranial tumors

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