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Age-related changes in blood and spleen-derived immune cells in long and short lived mice strains [RNA-seq]

ABSTRACT: 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).

ORGANISM(S): Mus musculus

PROVIDER: GSE159795 | GEO | 2021/12/01

REPOSITORIES: GEO

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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 | GSE159794 | GEO

Differences in PBMC mRNA profiles between control and type 2 diabetic mice

Project description:Studies on immunometabolism have indicated that metabolism and the immunological state are inherently interconnected . Recent research has highlighted the impacts of metabolic syndrome on innate and adaptive immune function, which are linked to overall negative effects on the progression of related diseases . Notably, aging of immune system can be potentiated by dysmetabolism, culminating in chronic inflammation and immune fitness loss . Several age-related immune changes such as progressive loss of naive T cells, an increase in memory cells, and increased percentages of cells with immunosenescence markers, were identified in patients with T2DM . Dysfunction of both innate and adaptive immune responses in T2DM manifests similarly to aging, including poor control of infection and reduced vaccination response, along with elevated inflammatory activity.Hence, we sought to investigate the mechanism of accelerated immunosenescence during T2DM.

2023-08-31 | GSE241618 | GEO

Lewkiewics2019 - effects of aging on naive T cell populations and diversity

Project description:This model is built by COPASI 4.24(Build197), based on paper: A mathematical model of the effects of aging on naive T-cell population and diversity Authors: Stephanie Lewkiewicz, Yao-li Chuang, Tom Chou Abstract: The human adaptive immune response is known to weaken in advanced age, resulting in increased severity of pathogen-born illness, poor vaccine efficacy, and a higher prevalence of cancer in the elderly. Age-related erosion of the T cell compartment has been implicated as a likely cause, but the underlying mechanisms driving this immunosenescence have not been quantitatively modeled and systematically analyzed. T cell receptor diversity, or the extent of pathogen-derived antigen responsiveness of the T cell pool, is known to diminish with age, but inherent experimental difficulties preclude accurate analysis on the full organismal level. In this paper, we formulate a mechanistic mathematical model of T cell population dynamics on the immunoclonal subpopulation level, which provides quantitative estimates of diversity. We define different estimates for diversity that depend on the individual number of cells in a specific immunoclone. We show that diversity decreases with age primarily due to diminished thymic output of new T cells and the resulting overall loss of small immunoclones.

2019-09-26 | BIOMD0000000824 | BioModels

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

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

2014-10-23 | GSE62580 | GEO

Epigenomics of Human CD8 T cell Differentiation and Aging

Project description:<p>The efficacy of the adaptive immune response declines dramatically with age, but the cell-intrinsic mechanisms driving the changes characteristic of immune aging in humans remain poorly understood. One hallmark of immune aging is the loss of self-renewing naive cells and the accumulation of differentiated but dysfunctional cells within the CD8 T cell compartment. Using ATAC-seq, we first inferred the transcription factor binding activities that maintain the naive and central and effector memory CD8 T cell states in young adults. Integrating our results with RNA-seq, we determined that BATF, ETS1, Eomes, and Sp1 govern transcription networks associated with specific CD8 T cell subset properties, including activation and proliferative potential. Extending our analysis to aged humans, we found that the differences between memory and naive CD8 T cells were largely preserved across age, but that naive and central memory cells from older individuals exhibited a shift toward a more differentiated pattern of chromatin openness. Additionally, aged naive cells displayed a loss in chromatin openness at gene promoters, a phenomenon that appears to be due largely to a loss in binding by NRF1, leading to a marked drop-off in the ability of the naive cell to initiate transcription of mitochondrial genes. Our findings identify BATF- and NRF1-driven gene regulation as targets for delaying CD8 T cell aging and restoring T cell function.</p>

| phs001187 | dbGaP

Age-specific variation in immune response in Drosophila melanogaster has a genetic basis.

Project description:Immunosenescence, the age-related decline in immune system function, is a general hallmark of aging. While much is known about the cellular and physiological changes that accompany immunosenescence, we know very little about the genetic influences on this phenomenon. We used microarrays to determine genome-wide expression profiles in twelve inbred D. melanogaster lines that varied in their ability to to clear an E. coli infection at one and four weeks of age.

2012-05-03 | GSE37708 | GEO

Global and tissue-specific aging effects on murine proteomes

Project description:Maintenance of protein homeostasis degrades with age, contributing to aging-related decline and disease. Previous studies have primarily surveyed transcriptional aging changes. To define the effects of age directly at the protein level, we perform discovery-based proteomics in 10 tissues from 20 C57BL/6J mice, representing both sexes at adult and late midlife ages (8 and 18 months). Consistent with previous studies, age-related changes in protein abundance often have no corresponding transcriptional change. Aging results in increases in immune proteins across all tissues, consistent with a global pattern of immune infiltration with age. Our protein-centric data reveal tissue-specific aging changes with functional consequences, including altered endoplasmic reticulum and protein trafficking in the spleen. We further observe changes in the stoichiometry of protein complexes with important roles in protein homeostasis, including the CCT/TriC complex and large ribosomal subunit. These data provide a foundation for understanding how proteins contribute to systemic aging across tissues.

2023-07-06 | PXD034029 | Pride

AginAging: a portrait from gene expression profile in blood cells: a portrait from gene expression profile in blood cells.

Project description:In almost every countries the proportion of people over 60 years is growing faster that any other age group. Increased life expectancy is leading to the characterization of specific aspects of aging for the various physiological systems. The study of healthy aging is important to design strategies capable to maximize the health and to prevent chronic diseases in older people. Immunosenscence reflects the age-related changes of the immune system and the reduced capacity of elderly people to cope with new infections. To elucidate changes in gene expression related to systemic aging and immunosenescence in an unbiased manner we performed comparative microarray analysis on whole blood cell from healthy middle-aged versus elderly men, and correlated results with functional measurements of aerobic capacity. Blood cells from elderly subjects showed age-related changes in the expression of several markers of immunosenescence, inflammation and oxidative stress, and showed impairments in metabolic and biosynthetic capacities.

2016-08-19 | GSE67220 | GEO

Effect of age on the arthritis susceptibility of BALB/c mice

Project description:Rheumatoid arthritis (RA) usually begins in females in their 4th-5th decade, suggesting that the aging of the immune system (immunosenescence) has a major impact on this disease. In the present microarray study, we set out to identify age- and arthritis-related gene expression pattern changes in proteoglycan (aggrecan)-induced arthritis (PGIA) model. Keywords: disease state analysis

2009-10-09 | GSE13148 | GEO

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