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A distinct priming phase regulates CD8 T cell immunity by orchestrating paracrine IL-2 signals

ABSTRACT: A distinct priming phase regulates CD8 T cell immunity by orchestrating paracrine IL-2 signals

PROVIDER: PRJNA1074275 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27900769_1.fastq.gz	Fastqsanger.gz
	SRR27900769_2.fastq.gz	Fastqsanger.gz
	SRR27900770_1.fastq.gz	Fastqsanger.gz
	SRR27900770_2.fastq.gz	Fastqsanger.gz
	SRR27900771_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

A distinct priming phase regulates CD8 T cell immunity by orchestrating paracrine IL-2 signals

Project description:T cell priming is characterized by an initial activation phase that involves long-term interactions with dendritic cells (DC). How paracrine signals are spatiotemporally transmitted once activated T cells have disengaged from DC and resumed their migration is currently unclear. Here, we identified a separate phase that serves to expand high-affinity CD8 T cells in specific subfollicular niches in lymph nodes. CD8 T cells required stop signals mediated by CXCR3 and a high affinity TCR to re-engage with antigen-laden DC in restricted microdomains. There, CD4 T cells delivered paracrine IL-2 in a stop-and-go migration pattern and thereby played an essential role in scaling primary CD8 T cell responses. Our results revise the current paradigm of T cell priming and have direct implications for vaccinations and cellular immunotherapies.

2025-04-11 | GSE255254 | GEO

WNT signals inhibit paracrine induction of senescence in human multipotent stromal cells

Project description:Senescence, the irreversible cell cycle arrest of damaged cells, is accompanied by a deleterious pro-inflammatory senescence-associated secretory phenotype (SASP). Senescence and the SASP are major factors in aging, cancer, and degenerative diseases, and interfere with the expansion of adult cells in vitro, yet little is known about how to counteract their induction and deleterious effects. Paracrine signals are increasingly recognized as important senescence triggers and understanding their regulation and mode of action may provide novel opportunities to reduce senescence-induced inflammation and improve cell-based therapies. Here, we show that the signalling protein WNT3A counteracts senescence in cultured human adult multipotent stromal cells (MSCs) by limiting paracrine senescence. We find that entry into senescence in a small subpopulation of MSCs triggers a secretome that causes a feed-forward signalling cascade that with increasing speed induces healthy cells into senescence. WNT signals interrupt this cascade by repressing cytokines that mediate this induction of senescence. Inhibition of those mediators by interference with NF-kB or interleukin 6 signalling reduced paracrine senescence in absence of WNT3A and promoted the expansion of MSCs. Our work reveals how WNT signals can antagonize senescence and has relevance not only for expansion of adult cells but can also provide new insights into senescence-associated inflammatory and degenerative diseases. // The RNAseq data in particular focusses on the transcriptome changes in MSCs occuring in vitro culture over four passages in presence or absence of growth factors WNT3A and FGF2.

2021-11-24 | GSE152112 | GEO

Decidual stromal cell response to paracrine signals from the trophoblast

Project description:During the invasive phase of implantation, trophoblasts and maternal decidual stromal cells secrete products that regulate trophoblast differentiation and migration into the maternal endometrium. Paracrine interactions between the extravillous trophoblast and the maternal decidua are important for successful embryonic implantation, including establishing the placental vasculature, anchoring the placenta to the uterine wall, and promoting immuno-acceptance of the fetal allograph. Global cross-talk between the trophoblast and the decidua has not been elucidated to date, and the current study used a functional genomics approach to investigate these paracrine interactions. Our data demonstrate a significant induction of pro-inflammatory cytokines and chemokines, as well as angiogenic/static factors in decidualized endometrial stromal cells in response to trophoblast-secreted products. The data suggest that the trophoblast acts to alter the local immune environment of the decidua to facilitate the process of implantation and assure an enriched cytokine/chemokine environment, while limiting mitotic activity of the stromal cells during the invasive phase of implantation. Keywords: Gene expression arrays in human stromal cells

2006-09-18 | GSE5809 | GEO

WNT signals inhibit paracrine induction of senescence in human multipotent stromal cells

Project description:WNT signals inhibit paracrine induction of senescence in human multipotent stromal cells

| PRJNA638361 | ENA

Tumor Explants Elucidate a Cascade of Paracrine SHH, WNT, and VEGF Signals Driving Pancreatic Cancer Angiosuppression

Project description:The sparse vascularity of Pancreatic Ductal Adenocarcinoma (PDAC) presents a mystery: what prevents this aggressive malignancy from undergoing neoangiogenesis to counteract hypoxia and better support growth? An incidental finding from prior work on paracrine communication between malignant PDAC cells and fibroblasts revealed that inhibition of the Hedgehog (HH) pathway partially relieved angiosuppression, increasing tumor vascularity through unknown mechanisms. Initial efforts to study this phenotype were hindered by difficulties replicating the complex interactions of multiple cell types in vitro. Here we identify a cascade of paracrine signals between multiple cell types that act sequentially to suppress angiogenesis in PDAC. Malignant epithelial cells promote HH signaling in fibroblasts, leading to inhibition of non-canonical WNT signaling in fibroblasts and epithelial cells, thereby limiting VEGFR2-dependent activation of endothelial hypersprouting. This cascade was elucidated using human and murine PDAC explant models, which effectively retain the complex cellular interactions of native tumor tissues.

2023-12-01 | GSE247072 | GEO

Modulating neutrophil phenotype via mesenchymal stromal cell paracrine signals insights from human and mouse experiments

Project description:Modulating neutrophil phenotype via mesenchymal stromal cell paracrine signals insights from human and mouse experiments

| PRJNA1212749 | ENA

Bypass of an epigenetic S-phase transcriptional module by convergent nutrient stress signals

Project description:The signals feeding into bacterial S-phase transcription are poorly understood. Cellular cycling in the alpha-proteobacterium Caulobacter crescentus is driven by a complex circuit of at least three transcriptional modules that direct sequential promoter firing during the G1, early and late S cell cycle phases. In alpha-proteobacteria, the transcriptional regulator GcrA and the CcrM methyltransferase epigenetically activate promoters of cell division and polarity genes that fire in S-phase. By evolving Caulobacter crescentus cells to cycle and differentiate in the absence of the GcrA/CcrM module, we discovered that phosphate deprivation and (p)ppGpp alarmone stress signals converge on S-phase transcriptional activation. The cell cycle oscillations of the CtrA protein, the transcriptional regulator CtrA that implements G1 and late S-phase transcription, are essential in our evolved mutants, but not in wild-type cells, showing that the periodicity in CtrA abundance alone can sustain cellular cycling without GcrA/CcrM. While similar nutritional sensing occurs in other alpha-proteobacteria, GcrA and CcrM are not encoded in the reduced genomes of obligate intracellular relatives. We thus propose that the nutritional stress response induced during intracellular growth obviated the need for an S-phase transcriptional regulator.

2023-11-09 | GSE135899 | GEO

Tumor Explants Elucidate a Cascade of Paracrine SHH, WNT, and VEGF Signals Driving Pancreatic Cancer Angiosuppression

Project description:Tumor Explants Elucidate a Cascade of Paracrine SHH, WNT, and VEGF Signals Driving Pancreatic Cancer Angiosuppression

| PRJNA1036165 | ENA

Priming

Project description:Priming

2025-05-29 | OEX00014296 | NODE

The impact of cold priming on the alerting phase of light and cold regulation of gene expression in Arabidopsis thaliana

Project description:We analysed the effect of a short 24 hours cold exposure (priming-stimulus) on gene regulation upon the first two hours of a second cold (4°C) stimulus (cold-triggering) and upon the first two hours of excess light exposure (800 µmol photons m-2 s-1, light triggering). The first and the second stress treatment was seperated by 5 days long lag-phase, which is long enough to reset most of the primary stress response. Several early light and early cold responsive genes showed however a altered transcript abundance in plants, which received five days befor the cold priming stimulus. Espicially JA responsive genes showed a common priming regulation within the cold and light exposure.

2021-06-25 | GSE162507 | GEO

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