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

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

PROVIDER: PRJNA1160824 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30659362_1.fastq.gz	Fastqsanger.gz
	SRR30659362_2.fastq.gz	Fastqsanger.gz
	SRR30659363_1.fastq.gz	Fastqsanger.gz
	SRR30659363_2.fastq.gz	Fastqsanger.gz
	SRR30659364_1.fastq.gz	Fastqsanger.gz

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

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

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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]

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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 [dnRA_Antag]

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

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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

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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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

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Autocrine TGF-β1 drives tissue-specific differentiation and function of resident NK cells

Project description:Group 1 innate lymphoid cells (ILCs) encompass NK cells and ILC1s which have non-redundant roles in host protection against pathogens and cancer. Despite their circulating nature, NK cells can establish residency in selected tissues during ontogeny, forming a distinct functional subset. The mechanisms that initiate, maintain, and regulate the conversion of NK cells into tissue-resident NK (trNK) cells are currently not well understood. Here, we identify autocrine transforming growth factor-b (TGF-b) as a cell-autonomous driver for NK cell tissue-residency across multiple glandular tissues during development. Cell-intrinsic production of TGF-β was continuously required for the maintenance of trNK cells and synergized with Hobit to enhance cytotoxic function. Whereas autocrine TGF-β was redundant in tumors, our study revealed that NK cell-derived TGF-β allowed expansion of cytotoxic trNK cells during local infection with murine cytomegalovirus (MCMV) and contributed to viral control in the salivary gland. Collectively, our findings reveal tissue-specific regulation of trNK cell differentiation and function by autocrine TGF-β1, which is relevant for anti-viral immunity.

2024-11-21 | GSE282148 | GEO

TGF-b-dependent Lymphoid Tissue Residency of Stem-like T cells Limits the Response to Tumor Vaccine

Project description:TGF-b-dependent Lymphoid Tissue Residency of Stem-like T cells Limits the Response to Tumor Vaccine

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