Functional T cells are capable of supernumerary cell division and longevity [ATAC-seq]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA880002 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR21542024_1.fastq.gz | Fastqsanger.gz | |||
| SRR21542024_2.fastq.gz | Fastqsanger.gz | |||
| SRR21542025_1.fastq.gz | Fastqsanger.gz | |||
| SRR21542025_2.fastq.gz | Fastqsanger.gz | |||
| SRR21542026_1.fastq.gz | Fastqsanger.gz |
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Project description:Functional T cells are capable of supernumerary cell division and longevity
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Project description:Functional T cells are capable of supernumerary cell division and longevity [RNA-seq]
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Project description:Differentiated somatic mammalian cells putatively exhibit species-specific division limits that impede cancer but may constrain lifespans. To provide immunity, transiently stimulated CD8 T cells undergo unusually rapid bursts of numerous cell divisions, then form quiescent long-lived memory cells that remain poised to reproliferate in response to subsequent immunological challenges. Here, we addressed whether T cells are intrinsically constrained by chronological or cell division limits. We activated mouse T cells in vivo using acute heterologous-prime-boost-boost vaccinations, transferred expanded cells to new mice, and then repeated that process iteratively. Over a period of 10 years (greatly exceeding the mouse lifespan) and 51 successive immunizations, T cells remained competent to respond to vaccination. Cells did require sufficient rest between stimulation events. Despite demonstrating the potential to expand the starting population at least 10^40-fold, cells did not show loss of proliferation control and results were not due to contamination with young cells. Persistent stimulation by chronic infections or cancer can result in a well-described transcriptional program that results in T cell proliferative senescence, functional exhaustion, and death. We found that while iterative acute stimulations also induced sustained expression and epigenetic remodeling of common exhaustion markers, including PD-1 and Tox, these cells retained the capacity to proliferate, execute antimicrobial functions, and form quiescent memory cells. These observations provide a model to better understand memory cell differentiation, exhaustion, and aging, and show that functionally competent T cells can retain the potential for extraordinary population expansion and longevity well beyond their organismal lifespan.
2022-11-17 | GSE213060 | GEO
Project description:Differentiated somatic mammalian cells putatively exhibit species-specific division limits that impede cancer but may constrain lifespans. To provide immunity, transiently stimulated CD8 T cells undergo unusually rapid bursts of numerous cell divisions, then form quiescent long-lived memory cells that remain poised to reproliferate in response to subsequent immunological challenges. Here, we addressed whether T cells are intrinsically constrained by chronological or cell division limits. We activated mouse T cells in vivo using acute heterologous-prime-boost-boost vaccinations, transferred expanded cells to new mice, and then repeated that process iteratively. Over a period of 10 years (greatly exceeding the mouse lifespan) and 51 successive immunizations, T cells remained competent to respond to vaccination. Cells did require sufficient rest between stimulation events. Despite demonstrating the potential to expand the starting population at least 10^40-fold, cells did not show loss of proliferation control and results were not due to contamination with young cells. Persistent stimulation by chronic infections or cancer can result in a well-described transcriptional program that results in T cell proliferative senescence, functional exhaustion, and death. We found that while iterative acute stimulations also induced sustained expression and epigenetic remodeling of common exhaustion markers, including PD-1 and Tox, these cells retained the capacity to proliferate, execute antimicrobial functions, and form quiescent memory cells. These observations provide a model to better understand memory cell differentiation, exhaustion, and aging, and show that functionally competent T cells can retain the potential for extraordinary population expansion and longevity well beyond their organismal lifespan.
2023-11-23 | GSE213229 | GEO
Project description:Differentiated somatic mammalian cells putatively exhibit species-specific division limits that impede cancer but may constrain lifespans1-3. To provide immunity, transiently stimulated CD8+ T cells undergo unusually rapid bursts of numerous cell divisions, and then form quiescent long-lived memory cells that remain poised to reproliferate following subsequent immunological challenges. Here we addressed whether T cells are intrinsically constrained by chronological or cell-division limits. We activated mouse T cells in vivo using acute heterologous prime-boost-boost vaccinations4, transferred expanded cells to new mice, and then repeated this process iteratively. Over 10 years (greatly exceeding the mouse lifespan)5 and 51 successive immunizations, T cells remained competent to respond to vaccination. Cells required sufficient rest between stimulation events. Despite demonstrating the potential to expand the starting population at least 1040-fold, cells did not show loss of proliferation control and results were not due to contamination with young cells. Persistent stimulation by chronic infections or cancer can cause T cell proliferative senescence, functional exhaustion and death6. We found that although iterative acute stimulations also induced sustained expression and epigenetic remodelling of common exhaustion markers (including PD1, which is also known as PDCD1, and TOX) in the cells, they could still proliferate, execute antimicrobial functions and form quiescent memory cells. These observations provide a model to better understand memory cell differentiation, exhaustion, cancer and ageing, and show that functionally competent T cells can retain the potential for extraordinary population expansion and longevity well beyond their organismal lifespan.
| S-EPMC11617068 | biostudies-literature
Project description:This SuperSeries is composed of the SubSeries listed below.
2022-11-17 | GSE213230 | GEO
Project description:The APETALA2-like transcription factor SUPERNUMERARY BRACT confers seed shattering by positively regulating qSH1 and SH5, while altering seed size by modulating longitudinal cell elongation in rice glumes.
2018-06-29 | GSE116422 | GEO
Project description:Despite extensive studies at the genomic, transcriptomic and metabolomic levels, the underlying mechanisms regulating longevity are incompletely understood. Post-translational protein acetylation is suggested to regulate aspects of longevity. To further explore the role of acetylation, we develop the PHARAOH computational tool based on the 100-fold differences in longevity within the mammalian class. Analyzing acetylome and proteome data across 107 mammalian species identifies 482 and 695 significant longevity-associated acetylated lysine residues in mice and humans, respectively. These sites include acetylated lysines in short-lived mammals that are replaced by permanent acetylation or deacetylation mimickers, glutamine or arginine, respectively, in long-lived mammals. Conversely, glutamine or arginine residues in short-lived mammals are replaced by reversibly acetylated lysine in long-lived mammals. Pathway analyses highlight the involvement of mitochondrial translation, cell cycle, fatty acid oxidation, transsulfuration, DNA repair and others in longevity. A validation assay shows that substituting lysine 386 with arginine in mouse cystathionine beta synthase, to attain the human sequence, increases the pro-longevity activity of this enzyme. Likewise, replacing the human ubiquitin-specific peptidase 10 acetylated lysine 714 with arginine as in short-lived mammals, reduces its anti-neoplastic function. Overall, in this work we propose a link between the conservation of protein acetylation and mammalian longevity.
2025-03-30 | PXD061654 | Pride
Project description:Glucose as a source of energy is centrally important to our understanding of life. We investigated the cell division-quiescence behavior of the fission yeast Schizosaccharomyces pombe under a wide range of glucose concentrations (0-111 mM). The mode of S. pombe cell division under a microfluidic perfusion system was surprisingly normal under highly diluted glucose concentrations (5.6 mM, 1/20 of the standard medium, within human blood sugar levels). Division became stochastic, accompanied by a curious division-timing inheritance, in 2.2-4.4 mM glucose. A critical transition from division to quiescence occurred within a narrow range of concentrations (2.2-1.7 mM). Under starvation (1.1 mM) conditions, cells were mostly quiescent and only a small population of cells divided. Under fasting (0 mM) conditions, division was immediately arrested with a short chronological lifespan (16 h). When cells were first glucose starved prior to fasting, they possessed a substantially extended lifespan (∼14 days). We employed a quantitative metabolomic approach for S. pombe cell extracts, and identified specific metabolites (e.g. biotin, trehalose, ergothioneine, S-adenosyl methionine and CDP-choline), which increased or decreased at different glucose concentrations, whereas nucleotide triphosphates, such as ATP, maintained high concentrations even under starvation. Under starvation, the level of S-adenosyl methionine increased sharply, accompanied by an increase in methylated amino acids and nucleotides. Under fasting, cells rapidly lost antioxidant and energy compounds, such as glutathione and ATP, but, in fasting cells after starvation, these and other metabolites ensuring longevity remained abundant. Glucose-starved cells became resistant to 40 mM H(2)O(2) as a result of the accumulation of antioxidant compounds.
2017-07-06 | MTBLS316 | MetaboLights