Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Age-related gene changes of naïve and memory T cells in a mouse age-tracking model

ABSTRACT: The transcriptomic changes of young and aged T cells are still unknown. Our previous study successfully tracked aged T cells generated from one wave of developing thymocytes of young age by a lineage-specific and inducible Cre-controlled reporter (TCRδCreERR26ZsGreen mouse strain). We used this transgenic mice and RNA-Seq to study the immunosenescence of naïve and memory T cell populations. A large number of genes involved in cellular and molecular functions, protein activity, cell cycle, cell adhesion, and immune functions were identified as having altered expression during aging. Our work revealed aged CD8 memory T cells with increased T cell activation and immunity genes, yet high expression of immunosuppressive checkpoints and resistance to cell death, implying aberrant T cell immunity in old mice. These feature genes identified in the current study serve as new therapeutic targets for correcting age-related defects.

ORGANISM(S): Mus musculus

PROVIDER: GSE163847 | GEO | 2020/12/25

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Homo sapiens

Project description:Immunosenescence: Immunity in the Young and Aged

| PRJNA258304 | ENA

Homo sapiens

Project description:Immunosenescence: Immunity in the Young and Aged

| PRJNA258303 | ENA

Age associated differences in microbiome in Rhesus Macaque

Project description:Aging is associated with declining immunity and inflammation as well as alterations in the gut microbiome with a decrease of beneficial microbes and increase in pathogenic ones. The aim of this study was to investigate aging associated gut microbiome in relation to immunologic and metabolic profile in a non-human primate (NHP) model. 12 old (age>18 years) and 4 young (age 3-6 years) Rhesus macaques were included in this study. Immune cell subsets were characterized in PBMC by flow cytometry and plasma cytokines levels were determined by bead based multiplex cytokine analysis. Stool samples were collected by ileal loop and investigated for microbiome analysis by shotgun metagenomics. Serum, gut microbial lysate and microbe-free fecal extract were subjected to metabolomic analysis by mass-spectrometry. Our results showed that the old animals exhibited higher inflammatory biomarkers in plasma and lower CD4 T cells with altered distribution of naïve and memory T cell maturation subsets. The gut microbiome in old animals had higher abundance of Archaeal and Proteobacterial species and lower Firmicutes than the young. Significant enrichment of metabolites that contribute to inflammatory and cytotoxic pathways was observed in serum and feces of old animals compared to the young. We conclude that aging NHP undergo immunosenescence and age associated alterations in the gut microbiome that has a distinct metabolic profile.

2022-02-01 | E-MTAB-10160 | biostudies-arrayexpress

Transcription profiling of C57BL/6NIA mouse hippocampus to survey age-related changes in mRNA levels.

Project description:We carried out a global survey of age-related changes in mRNA levels in the C57BL/6NIA mouse hippocampus and found a difference in the hippocampal gene expression profile between 2-month-old young mice and 15-month-old middle-aged mice correlated with an age-related cognitive deficit in hippocampal-based explicit memory formation. Middle-aged mice displayed a mild but specific deficit in spatial memory in the Morris water maze. Experiment Overall Design: No technical replicates; 14 biological replicates for 15-month-old mice, 9 biological replicates for 2-month-old mice. Whole hippocampus.

2007-11-27 | E-GEOD-5078 | biostudies-arrayexpress

Correction of age-associated defects in dendritic cell functions enables CD4+T cells to eradicate tumors in the elderly

Project description:Defective host defenses later in life are associated with changes in immune system activity. The means to correct immune defects to ensure immunity in the elderly are undefined. In this study, we found that CD8+T cells, which are necessary for anti-tumor immunity in young mice, are not required to eradicate the same cancers later in life. Rather, CD4+T cells drive anti-tumor immunity in elderly mice. The generation of anti-tumor CD4+T cells requires multiple dendritic cell (DC) activities that are elicited by immune agonists known as hyperactivators, but not by adjuvants that model those used clinically. DC hyperactivators correct age-associated defects in DC migration and T cell co-stimulation while enabling NLRP3 inflammasome activities within living cells. These combined activities enable DCs to induce TH1-skewed T cells that persist into old age and eliminate implantable tumors. These results raise the possibility of correcting age-associated immune defects through DC manipulation.

2024-06-12 | GSE260791 | GEO

Age-associated loss of lamin-B leads to systemic inflammation and gut hyperplasia

Project description:Aging of immune organs, termed as immunosenescence, is suspected to promote systemic inflammation and age-associated disease. The cause of immunosenescence and how it promotes disease, however, has remained unexplored. We report that the Drosophila fat body, a major immune organ, undergoes immunosenescence and mounts strong systemic inflammation that leads to de-regulation of immune deficiency (IMD) signaling in the midgut of old animals. Inflamed old fat bodies secrete circulating peptidoglycan recognition proteins that repress IMD activity in the midgut, thereby promoting gut hyperplasia. Further, fat body immunosenecence is caused by ageassociated lamin-B reduction specifically in fat body cells, which then contributes to heterochromatin loss and de-repression of genes involved in immune responses. As lamin-associated heterochromatin domains are enriched for genes involved in immune response in both Drosophila and mammalian cells, our findings may provide insights into the cause and consequence of immunosenescence during aging. 17 samples from the fat body, the midgut, or the whole gut with different ages or RNAi treatment. 6 of the samples were wildtype young control. For each experiment, we had two or three biological replicates.

2014-10-23 | E-GEOD-62580 | biostudies-arrayexpress

Transcription profiling of rat hippocampus from young and aged rats with age-related spatial learning impairments

Project description:The aim of this study was to investigate whether the differences in memory decline associated with aging are a result of differences in gene expression. We first categorized age-unimpaired and age-impaired rats based on their performance in the Morris Water Maze and then isolated messenger RNA from the CA1 hippocampal region of each animal to interrogate Affymetrix microarrays. Microarray analysis (p<0.005) identified a set of 50 genes that were transcribed differently in age-unimpaired animals that had successfully learned a spatial task compared to aged learning-impaired animals and a variety of groups designed to control for all non-learning aspects of exposure to the water maze paradigm. Experiment Overall Design: a total of 79 samples were analyzed including aged and young rats. One chip was interrogated per animal. Analysis of aged rat data includes 44 samples. Controls include cage controls, yoked controls (no platform), visible platform controls.

2007-11-06 | E-GEOD-3531 | biostudies-arrayexpress

Project description:Immune system aging contributes significantly to declining health with age. It is unknown to what extent human and mice immune systems go through similar age-related changes and whether there are conserved biomarkers of aging. We characterized age-related changes in the immune system of long (C57BL/6J) and short-lived (NZO/HILtJ) strains and compared them with blood-driven human aging signatures. Peripheral blood lymphocytes (PBL), spleen cells and spleen-driven naive and memory CD8+ T cells were profiled using flow cytometry, RNA-seq and ATAC-seq from young (3 months) and old (18 months) mice. Pro-inflammatory myeloid genes were activated with age across strains and tissues, echoing human 'inflammaging' signatures. ATAC-seq footprinting analyses uncovered increased binding of pro-inflammatory transcription factors with age (e.g., AP1 complex, NFKB signaling pathway). Machine learning models identified inflammation, cytotoxic, and naive T cell derived genes to be strong signatures of immunosenescence. These data are publicly shared as a resource for immune aging (https://immune-aging.jax.org/mice).

2021-12-01 | GSE159795 | GEO

2021-12-01 | GSE159794 | GEO

Restoring Systemic GDF11 Levels Reverses Age-Related Dysfunction in Mouse Skeletal Muscle

Project description:In this study, we investigated signaling pathways in Skeletal muscle precursors that are altered with aging and age-related deficits in muscle regenerative potential. We performed fluorescence activated cell sorting (FACS) to obtain highly purified skeletal muscle satellite cells from young, middle-aged and old mice. Parabiosis experiments indicate that impaired regeneration in aged mice is reversible by exposure to a young circulation, suggesting that young blood contains humoral "rejuvenating" factors that can restore regenerative function. Here, we demonstrate that the circulating protein growth differentiation factor 11 (GDF11) is a rejuvenating factor for skeletal muscle. Supplementation of systemic GDF11 levels, which normally decline with age, by heterochronic parabiosis or systemic delivery of recombinant protein, reversed functional impairments and restored genomic integrity in aged muscle stem cells (satellite cells). Increased GDF11 levels in aged mice also improved muscle structural and functional features and increased strength and endurance exercise capacity. These data indicate that GDF11 systemically regulates muscle aging and may be therapeutically useful for reversing age-related skeletal muscle and stem cell dysfunction. We used Affymetrix Mouse Genome array to identify global transcriptional changes associated with age in skeletal muscle precursors.

2014-05-08 | E-GEOD-50821 | biostudies-arrayexpress