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Retinoic acid and TGF-β orchestrate organ-specific programs of tissue-residency [dnRA_Antag]

ABSTRACT: Retinoic acid and TGF-β orchestrate organ-specific programs of tissue-residency [dnRA_Antag]

PROVIDER: PRJNA1161493 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30674079.fastq.gz	Fastqsanger.gz
	SRR30674080.fastq.gz	Fastqsanger.gz
	SRR30674081.fastq.gz	Fastqsanger.gz
	SRR30674082.fastq.gz	Fastqsanger.gz
	SRR30674083.fastq.gz	Fastqsanger.gz

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Retinoic acid and TGF-β orchestrate organ-specific programs of tissue-residency

Project description:Retinoic acid and TGF-β orchestrate organ-specific programs of tissue-residency

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Retinoic acid and TGF-β orchestrate organ-specific programs of tissue-residency [dnRARa]

Project description:Retinoic acid and TGF-β orchestrate organ-specific programs of tissue-residency [dnRARa]

| PRJNA1161491 | ENA

Retinoic acid and TGF-β orchestrate organ-specific programs of tissue-residency

Project description:Tissue-resident memory T (TRM) cells are integral to tissue immunity, persisting in diverse anatomical sites where they adhere to a common transcriptional framework. How these cells integrate distinct local cues to adopt the common TRM cell fate remains poorly understood. Here, we show that while skin TRM cells strictly require TGF-β for tissue residency, those in other locations utilize the metabolite retinoic acid (RA) to drive an alternative differentiation pathway, directing a TGF-β-independent tissue residency program in the liver and synergizing with TGF-β to drive the TRM cells in the small intestine.

2024-09-16 | GSE277120 | GEO

Retinoic acid and TGF-β orchestrate organ-specific programs of tissue-residency [dnRARa]

2024-09-16 | GSE277247 | GEO

Retinoic acid and TGF-β orchestrate organ-specific programs of tissue-residency [dnRA_Antag]

2024-09-16 | GSE277248 | GEO

Comparative analysis reveals a role for TGF-β in shaping the residency-related transcriptional signature in tissue-resident memory CD8+ T cells

Project description:Tissue-resident CD8+ memory T (TRM) cells are immune cells that permanently reside at tissue sites where they play an important role in providing rapid protection against reinfection. They are not only phenotypically and functionally distinct from their circulating memory counterparts, but also exhibit a unique transcriptional profile. To date, the local tissue signals required for their development and long-term residency are not well understood. So far, the best-characterised tissue-derived signal is transforming growth factor-β (TGF-β), which has been shown to promote the development of these cells within tissues. In this study, we aimed to determine to what extent the transcriptional signatures of TRM cells from multiple tissues reflects TGF-β imprinting. We activated murine CD8+ T cells, stimulated them in vitro by TGF-β, and profiled their transcriptomes using RNA-seq. Upon comparison, we identified a TGF-β-induced signature of differentially expressed genes between TGF-β-stimulated and -unstimulated cells. Next, we linked this in vitro TGF-β-induced signature to a previously identified in vivo TRM-specific gene set and found considerable (>50%) overlap between the two gene sets, thus showing that a substantial part of the TRM signature can be attributed to TGF-β signalling. Finally, gene set enrichment analysis further revealed that the altered gene signature following TGF-β exposure reflected transcriptional signatures found in TRM cells from both epithelial and non-epithelial tissues. In summary, these findings show that TGF-β has a broad footprint in establishing the residency-specific transcriptional profile of TRM cells, which is detectable in TRM cells from diverse tissues. They further suggest that constitutive TGF-β signaling might be involved for their long-term persistence at tissue sites.

2019-01-23 | GSE125471 | GEO

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

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.

2022-05-24 | GSE182511 | GEO

Lysosome-targeting chimeras based on retinoic acid modification for cancer therapy

Project description:We developed retinoic acid-based LYTACs (RATACs) to overcome synthesis and druggability issues. RATACs degrade EGFR, PD-L1, TGF-β, and IgG, showing superior anti-tumor effects in liver and lung cancer models compared to conventional antibodies.

2025-07-14 | PXD066144 |

Whole-organ analysis of TGF-b-mediated remodelling of the tumour microenvironment

Project description:Whole-organ analysis of TGF-b-mediated remodelling of the tumour microenvironment

| PRJNA642788 | ENA