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Transcriptomic analysis of resting or activated human CD226- and CD226+ effector memory CD8+ T cell subsets isolated from the peripheral blood of healthy donors.

ABSTRACT: Transcriptomic analysis of resting or activated human CD226- and CD226+ effector memory CD8+ T cell subsets isolated from the peripheral blood of healthy donors.

PROVIDER: PRJNA551394 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9606450_1.fastq.gz	Fastqsanger.gz
	SRR9606450_2.fastq.gz	Fastqsanger.gz
	SRR9606460_1.fastq.gz	Fastqsanger.gz
	SRR9606460_2.fastq.gz	Fastqsanger.gz
	SRR9606451_1.fastq.gz	Fastqsanger.gz

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Transcriptomic analysis of resting or activated human CD226- and CD226+ effector memory CD8+ T cell subsets isolated from the peripheral blood of healthy donors.

Project description:We recently found that loss of the activating receptor CD226 (DNAM-1) was a critical mechanism affecting CD8+ T cell responsiveness to TCR stimulation. To better understand the molecular differences between CD226- and CD226+ CD8+ T cells, we decided to perform a global transcriptional analysis of purified CD226+ and CD226- CD8+ effector memory T cells before and after TCR activation using next generation RNA sequencing. We report here the total RNA sequencing of healthy donor resting CD226- and CD226+ CD8+ Tem cells (n=6/group) or activated (ACT, n=4/group) by α-CD2/CD3/CD28 for 24 hrs.

2020-10-30 | GSE133397 | GEO

Transcriptomic analysis of freshly purified human CD226- and CD226+ CD8+ T cell subsets isolated from the peripheral blood of healthy donors.

Project description:We recently found that loss of the activating receptor CD226 (DNAM-1) was a critical mechanism affecting CD8+ T cell responsiveness to TCR stimulation. To better understand the molecular differences between CD226- and CD226+ CD8+ T cells, we decided to perform a global transcriptional analysis of purified naive (Tn, CD62L+CD45RA+), central memory (Tcm, CD62L+CD45RA-) and terminal effector memory (Temra, CD62L-CD45RA+) CD226+ and CD226- CD8+ T cells using next generation RNA sequencing.

2020-10-30 | GSE135291 | GEO

Blocking CD226 regulates ILC2 effector function and alleviates airway hyperreactivity

Project description:Type 2 innate lymphoid cells (ILC2s) play a pivotal role in type 2 asthma. CD226 is a costimulatory molecule involved in various inflammatory diseases. Here, we aimed to investigate CD226 expression and function within human and mouse ILC2s, and to assess the impact of targeting CD226 on ILC2-mediated airway hyperreactivity (AHR). Our findings demonstrated an inducible expression of CD226 in activated ILC2s, enhancing their cytokine secretion and effector functions. Blocking CD226 ameliorates ILC2-dependent AHR in IL-33 and Alternaria Alternata-induced models. Interestingly, CD226 is expressed and inducible in human ILC2s, and its blocking reduces cytokine production. Finally, we showed that peripheral ILC2s in asthmatic patients exhibited elevated CD226 expression compared to healthy controls.Our findings underscore the potential of CD226 as a novel therapeutic target in ILC2s, presenting a promising avenue for ameliorating AHR and allergic asthma.

2024-04-16 | GSE264060 | GEO

Transcriptomic analysis of freshly purified human CD226- and CD226+ CD8+ T cell subsets isolated from the peripheral blood of healthy donors.

Project description:Transcriptomic analysis of freshly purified human CD226- and CD226+ CD8+ T cell subsets isolated from the peripheral blood of healthy donors.

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Increased CD226 Expression on CD8+ T cells in Patients with Systemic Sclerosis

Project description:Systemic sclerosis (SSc) is an autoimmune disease characterized by vascular damage, and fibrosis of the skin and internal organs. Because activated and oligoclonally expanded CD8+ T cells can be detected in peripheral blood and lung of SSc patients, effector memory CD8+ T cells may play a critical role for organ involvement in SSc; however, the pathogenic functions of effector memory CD8+ T cells remain incompletely understood. Here we performed DNA microarray analysis of the sort-purified effector memory CD8+ T cells from SSc patients and healthy controls, and showed that the expression of genes related to immune response and cell adhesion, including CD226 (also known as DNAX accessory molecule-1, DNAM-1), was significantly altered. Moreover, detailed analysis of CD226 revealed that CD226highCD8+ T cells were increased in SSc patients (mean, 50.7%) compared with healthy controls (32.9%) and were appreciably associated with the severity of skin sclerosis and interstitial lung disease. Further, CD226highCD8+ T cells from SSc patients produced abundant IL-13 and were positively correlated with the cytotoxic capacity of CD8+ T cells against HUVECs. Finally, the neutralization of CD226 impaired IL-13 production and cytolysis against HUVECs. These findings indicate that upregulated CD226 expression on CD8+ T cells reflects disease severity and are involved in SSc pathogenesis via the production of profibrotic IL-13 and endothelial cell injury, and that CD226 may be a useful target in the treatment of SSc. We first purified effector memory CD8+ T cells (CD3+CD8+CD45RO+CD62L+ cells) from peripheral blood by cell sorting and subsequently performed cDNA microarray analysis of the sort-purified effector memory CD8+ T cells from 9 SSc patients and 5 healthy controls.

2014-12-06 | E-GEOD-63903 | biostudies-arrayexpress

Monoclonal Antibody Blockade of CD226 Decreases Spontaneous Diabetes in the NDO Mouse by Augmenting Treg and Diminishing Effector Functionality

Project description:Immunotherapeutics that modulate T cell activation represent a crucial component for inhibiting the autoimmune pathogenesis of type 1 diabetes (T1D) and improving the efficacy of β-cell replacement therapy. Here, we present a novel strategy for reducing diabetes incidence in the NOD mouse using monoclonal antibodies (mAbs) to block the T cell costimulatory receptor, CD226. Notably, female NOD mice treated with 600 µg of ⍺-CD226 mAbs between 7-8 weeks of age showed decreased disease incidence at 30 weeks and reduced insulitis severity compared to mice treated with an isotype control. Ex vivo analysis performed five weeks post-treatment revealed ⍺-CD226 mAbs persist in vivo, reducing the availability of CD226 on CD8+ T cells and Tregs. Flow cytometric analysis demonstrates that ⍺-CD226 mAbs inhibit the proliferation of both CD4+ and CD8+ T cells in vitro. Similarly, ex vivo samples had reduced CD4+ and CD8+ effector memory T cell proliferation following ⍺-CD226 mAb treatment. Splenocytes treated with ⍺-CD226 mAbs exhibited a more immunoregulatory cytokine profile with decreased IFN-γ and increased IL-10 production. This phenotype was further corroborated by 51Cr-release assays demonstrating reduced cell-mediated lympholysis (CML) of murine β-cells by ⍺-CD226 mAb-treated autoreactive cytotoxic lymphocytes. Ex vivo phenotyping of FOXP3+Helios+ Tregs revealed increased CD25 expression following ⍺-CD226 mAb treatment, with Tregs displaying augmented suppressive capacity of CD4+ responders during in vitro suppression assays. These data suggest that ⍺-CD226 mAbs both reduce T cell cytotoxicity and improve Treg function, with important therapeutic implications for the prevention or suspension of T1D.

2024-08-16 | GSE254403 | GEO

Blocking CD226 regulates ILC2 effector function and alleviates airway hyperreactivity

Project description:Blocking CD226 regulates ILC2 effector function and alleviates airway hyperreactivity

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Genome-wide ATAC-seq maps in human Treg subsets and CD4+ T effector cells

Project description:We report the application of ATAC-seq to flow sorted Foxp3+Helios+ memory and naïve regulatory T cell subsets and memory CD4+ T effector cells in both resting condition and after in vitro stimulation (4 hours) with PMA/Ionomycin.

2022-10-04 | GSE173607 | GEO

Transcriptional profiles of CCR7lo effector memory human T cell subsets

Project description:The aim of this study was to identify differentially-expressed genes in CCR4hi/CXCR3- and CCR4lo CXCR3+ CCR6+ human Th17 cell subsets Human CD45RO+ memory T cells isolated from the peripheral blood of healthy adult donors were sorted into 4 predominant CCR7lo CD25- effector memory subsets: (1) Th1 - CCR6- CCR4lo CXCR3+; (2) Th2 - CCR6- CCR4hi CXCR3+; (3) Th17 - CCR6+ CCR4hi CXCR3-; (4) Th17.1 - CCR6+ CCR4lo CXCR3-. Sorted cells were cultured in media and activated via anti-CD3/anti-CD28 beads for 36 hours. All subsets were then harvested and used for RNA extraction and microarray experiments. Th1 vs Th2; Th1 vs Th17; Th1 vs Th17.1; Th2 vs Th17; Th2 vs Th17.1; Th17 vs Th17.1

2013-12-17 | E-GEOD-49703 | biostudies-arrayexpress

Increased CD226 Expression on CD8+ T cells in Patients with Systemic Sclerosis

2014-12-06 | GSE63903 | GEO