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Characterization of young and aged lung tissue-resident influenza nucleoprotein-specific CD8 memory T cells

ABSTRACT: To identify the disparaties of D^b-nucleoprotein specific resident memory CD8 T cells between young and aged mice, we pooled n=11 aged or n=18 young lungs together after intraveounously labeling T cells and sorted ivCD90- CD8a+ CD44hi CD69+ D^b-NP tetramer (PE+ & APC+) cells. By scRNA-seq, we found the aged population was missing a cluster in the young population that resembled typical functional resident memory CD8 T cells indicating that aged resident memory CD8 T cells of this specificity would have poor recall function.

ORGANISM(S): Mus musculus

PROVIDER: GSE159065 | GEO | 2020/10/06

REPOSITORIES: GEO

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Characterization of young and aged lung tissue-resident influenza nucleoprotein-specific CD8 memory T cells

Project description:Characterization of young and aged lung tissue-resident influenza nucleoprotein-specific CD8 memory T cells

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scRNA-seq analysis of mouse splenic CD8 T cells 1 month post transfer of CD8 T cells from 3 months old donor into 24 months old recipient

Project description:Aging is associated with systemic chronic inflammation (inflammaging) that leads to impaired physiological functions and vulnerability to several diseases. However, underlying alterations in aged immune system resulting in gradual loss of immune fitness remain unclear. Using a combination of CD8 T cell transfer from young to old and from old to young mice and single-cell RNA sequencing, we characterized the age-associated alterations in CD8 T cells. We transferred 2 millions of purified CD8+ T cells pooled from 3 CD45.1 C57BL/6J 3 months old female mice (donor) by i.v. injection into CD45.2 C57BL/6J 24 months old female mouse (recipient) and sorted CD45.1+CD3e+CD8a+ and CD45.2+CD3e+CD8a+ T cells from the spleen 1 month post transfer to perform scRNA/TCR-seq.

2020-12-06 | GSE155005 | GEO

The impact of aging on memory T cell phenotype and function in the human bone marrow

Project description:Recently, the bone marrow (BM) has been shown to play a key role in regulating the survival and function of memory T cells. However, the impact of aging on these processes has not yet been studied. We demonstrate that the number of CD4+ and CD8+ T cells in the BM is maintained during aging. However, the composition of the T cell pool in the aged BM is altered with a decline of naïve and an increase in effector-memory T cells. In contrast to the peripheral blood (PB), a highly activated CD8+CD28– T cell population, which lacks the late differentiation marker CD57, accumulates in the BM of elderly persons. IL-6 and IL-15, which are both increased in the aged BM, efficiently induce the activation, proliferation and differentiation of CD8+ T cell in vitro, highlighting a role of these cytokines in the age-dependent accumulation of highly activated CD8+CD28– T cells in the BM. Yet, these age-related changes do not impair the maintenance of a high number of polyfunctional memory CD4+ and CD8+ T cells in the BM of elderly persons. In summary, aging leads to the accumulation of a highly activated CD8+CD28– T cell population in the BM, which is driven by the age-related increase of IL-6 and IL-15. Despite these changes, the aged BM is a rich source of polyfunctional memory T cells and may thus represent an important line of defense to fight recurrent infections in old age. A total of 4 samples (bone marrow mononuclear cells) were analyzed (2 young and 2 elderly persons)

2011-10-11 | E-GEOD-32725 | biostudies-arrayexpress

Comparison of young and aged mouse CD8 TN, TVM and TMEM cells directly ex vivo and after polyclonal stimulation

Project description:The overall study (Quinn et al. Cell Reports, 2018) aimed to understand why CD8 virtual memory T (TVM) cells become markedly less proliferative in response to TCR-driven signals with increasing age, whereas CD8 true naive (TN) cells maintain their proliferative capacity. Age-associated decreases in primary CD8+ T cell responses occur, in part, due to direct effects on naïve CD8++ T cells to reduce intrinsic functionality, but the precise nature of this defect remains undefined. Ageing also causes accumulation of antigen-naïve but semi-differentiated “virtual memory” (TVM) cells but their contribution to age-related functional decline is unclear. Here, we show that TVM cells are poorly proliferative in aged mice and humans, despite being highly proliferative in young individuals, while conventional naïve T cells (TN cells) retain proliferative capacity in both aged mice and humans. Adoptive transfer experiments in mice illustrated that naïve CD8 T cells can acquire a proliferative defect imposed by the aged environment but age-related proliferative dysfunction could not be rescued by a young environment. Molecular analyses demonstrate that aged TVM cells exhibit a profile consistent with senescence, marking the first description of senescence in an antigenically naïve T cell population.

2018-06-19 | GSE112304 | 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>

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Characterization of resident CD8+ Trm cell populations using whole-genome biomarker analysis

Project description:This study seeks a better understanding of the functional differences between naturally acquired murine CD8+ T resident memory (Trm) cells of three distinct mucosal environments; the small intestine, the lung and the liver. CD8+ Trm cells of healthy young adult mice were retrieved from their respective organ environments by automated organ disintegration and MACS sorting, and compared with each other by whole genome gene expression profiling. Peripheral blood derived circulating CD8+ Tem cells were also analyzed, serving as nonresident peripheral memory T cell controls, in an attempt to identify common characteristics of resident mucosal CD8+ Trm subsets, as well.

2019-01-04 | GSE65044 | GEO

Project description:Tissue resident memory CD8 T cells

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The Aryl Hydrocarbon Receptor Cell-Intrinsically Promotes Resident Memory CD8+ T Cell Differentiation and Function

Project description:The Aryl hydrocarbon receptor (Ahr) regulates the differentiation and function of CD4+ T cells; however, the cell-intrinsic role of Ahr in CD8+ T cells, remains elusive. Herein we show that Ahr acts as a promoter of resident memory CD8+ T cell (TRM) differentiation and function. Under steady state conditions or in an oral infection model, genetic ablation of Ahr in CD8+ T cells leads to an increase in CD127–KLRG1+ short lived effector cells (TSLE) and CD44+CD62L+ T central memory (TCM) cells, but a reduction in Granzyme B-producing CD69+CD103+ T resident memory (TRM) cells. Genome-wide transcriptome and cistrome analyses reveal that Ahr suppresses the circulating while promoting the resident memory core gene program. A tumor resident polyfunctional CD8+ T cell population dependent on Ahr is revealed by single cell RNA-Seq, and deletion of Ahr in CD8+ T cells compromises anti-tumor immunity. Consistent with mouse, human IEL CD8+ T cells highly express AHR that regulates in vitro TRM differentiation and Granzyme B production. Collectively, these data suggest that Ahr is an important cell-intrinsic factor for CD8+ T cell immunity.

2023-01-11 | GSE220944 | GEO

Transcriptional profiling of CD8 cells laser captured from skin biopsies at dermal-epidermal junction and at deeper dermal area near blood vessel during the healed phase of mucocutaneous HSV-2 reactivation

Project description:We aim to get a comprehensive analysis on gene expression of CD8a+ T-cells during the post healed phases of HSV-2 reactivation at different anatomic location (CD8a+ cells at dermal-epidermal junction versus CD8a+ cells in deeper dermal area near blood vessel). Our hypothesis is that JC_CD8 cells may function as a resident effector-like T-cells while BV_CD8 cells may be infiltrating cells from circulation. CD8 cells were immunofluorescently stained and laser captured from genital skin biopsies at dermal-epidermal junction at 2 and 8 weeks post healed (JC_2wks_CD8 and JC_8wks_CD8) and at deeper dermal area near blood vessel (BV_2wks_CD8 and BV_8wks_CD8); total RNA were purified from captured cells and cDNA were amplified from the total RNA using NuGEN pico kits

2013-04-11 | E-GEOD-44975 | biostudies-arrayexpress

Targeting pathogenic CD8+ tissue-resident T cells with chimeric antigen receptor therapy in murine autoimmune cholangitis

Project description:Primary biliary cholangitis (PBC) is a cholestatic autoimmune liver disease secondary to an autoreactive T cell response against intrahepatic small bile ducts. Multiple murine models have demonstrated the critical role of effector CD8+T cells in this response and our work has used IL-12p40-/-IL-2Rα-/- mice (DKO mice) to study this issue. Herein we first demonstrated that use of either a CD8a knock-out or an anti-CD8a antibody prevents/reduces biliary immunopathology. Bulk and single-cell RNA sequencing analysis identifies CD8+ tissue resident memory T cells (Trm) in the liver of DKO mice, which highly express activation and cytotoxicity associated markers and have the ability to induce apoptosis of bile duct epithelial cells. Liver CD8+Trm cells also upregulate expression of several immune checkpoint molecules and in particular we identified PD-1 as a specific liver CD8+Trm cell marker in this model. Based on these data we constructed a novel chimeric antigen receptor containing a PD-L1 extracellular domain to target PD-1-expressing CD8+Trm cells. Importantly, treatment of DKO mice with PD-1 targeting CAR-T cells selectively depleted liver CD8+Trm cells in vivo and alleviated autoimmune cholangitis.

2023-09-05 | GSE241014 | GEO

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