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Calcitonin gene-related peptide sustains CD8 T cell inflammatory reactions in drug -induced reactions [CD8 Smart-seq]

ABSTRACT: Calcitonin gene-related peptide sustains CD8 T cell inflammatory reactions in drug -induced reactions [CD8 Smart-seq]

PROVIDER: PRJNA1047005 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26993700_1.fastq.gz	Fastqsanger.gz
	SRR26993700_2.fastq.gz	Fastqsanger.gz
	SRR26993689_1.fastq.gz	Fastqsanger.gz
	SRR26993689_2.fastq.gz	Fastqsanger.gz
	SRR26993690_1.fastq.gz	Fastqsanger.gz

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Calcitonin gene-related peptide sustains CD8 T cell inflammatory reactions in drug -induced reactions

Project description:Calcitonin gene-related peptide sustains CD8 T cell inflammatory reactions in drug -induced reactions

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Calcitonin gene-related peptide sustains CD8+ T cell inflammatory reactions in drug -induced reactions [scRNA-Seq]

Project description:Calcitonin gene-related peptide sustains CD8+ T cell inflammatory reactions in drug -induced reactions [scRNA-Seq]

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Calcitonin gene-related peptide sustains CD8 T cell inflammatory reactions in drug -induced reactions [CD8 Smart-seq]

Project description:We investigated the differentiation pattern induced by CGRP on CD8+ T cells

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Calcitonin gene-related peptide sustains CD8+ T cell inflammatory reactions in drug -induced reactions [scRNA-Seq]

Project description:We investigated the differentiation pattern of CD8+ T cells from healthy controls and patients with SJS/TEN.

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Calcitonin gene-related peptide sustains CD8 T cell inflammatory reactions in drug -induced reactions

Project description:This SuperSeries is composed of the SubSeries listed below.

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Krüppel-like factor 4 regulates the cytolytic effector function of exhausted CD8 T-cells [SMART-Seq]

Project description:To identify the role of KLF4 on exhausted CD8 T-cells in vivo, we adoptively transferred PmelI CD8 T-cells transduced with MigRI/Klf4 into MC38-gp100 tumor-bearing Rag2 KO mice on day7. We then isolated tumor-infiltrating PmelI CD8 T-cells on day15 and their gene expression profiles were analyzed by SMART-seq. Also, to investigate the effect of KLF4 deficiency, we isolated PD1+ CD8+ TILs from MC38 tumor-bearing control and Klf4 cKO mice on day14, and SMART-seq was performed.

2022-10-24 | GSE212803 | GEO

Single-cell RNA-seq analysis of human KIR+ CD8 T cells by Smart-seq2

Project description:KIR+ CD8 T cells (Live CD3+CD56-TCRab+CD8+KIR+ cells) were sorted from the blood of healthy subjects (N=10) and patients with MS (N=2), SLE (N=6), or CeD (N=5) and subjected to single-cell RNA-seq analysis by Smart-seq2. In parallel, we also analyzed their T-cell receptor (TCR) α and β sequences. Unsupervised clustering of these KIR+CD8+ T cells by Seurat identified six clusters, with Clusters 1 to 3 mostly containing expanded KIR+CD8+ T cells (≥2 cells expressing same TCR) and Clusters 5 and 6 consisting of unexpanded cells expressing unique TCRs. There are common features shared by KIR+CD8+ T cells from healthy subjects and different diseases, yet there is also heterogeneity (i.e., upregulated type I IFN signaling and glycolysis in Clusters 2 and 3) associated with different diseases or treatments.

2022-03-08 | GSE193439 | GEO

SMART-seq of PD1+ and PD1- CD8 T cells derived from Setx L389S (Setx KI) mice

Project description:The goal is to understand the nature of PD-1+ CD8 T cells that are detected in the peripheral blood of ALS4 mice (expressing the mutation SetxL389S, also called Setx KI mice). We performed a SMART (Switching Mechanism At the end of the 5’-end of the RNA Transcript)-sequencing analysis of the transcriptome of effector memory CD8 T cells expressing or not PD-1 from the blood of symptomatic KI animals. Amongst the transcripts differentially expressed between these two populations, we detected upregulation of Tox (Thymocyte Selection Associated High Mobility Group Box) in PD-1+ as compared to PD-1- CD8 T cells.

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Bromodomain protein BRD4 directs and sustains CD8 T cell differentiation during infection

Project description:Bromodomain protein BRD4 directs and sustains CD8 T cell differentiation during infection

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Calcitonin controls bone formation by inhibiting the release of sphingosine 1-phosphate from osteoclasts

Project description:The hormone calcitonin (CT) is primarily known for its pharmacologic action as an inhibitor of bone resorption, yet CT-deficient mice display increased bone formation. These findings raised the question about the underlying cellular and molecular mechanism of CT action. Here we show that either ubiquitous or osteoclast-specific inactivation of the murine CT receptor (CTR) causes increased bone formation. CT negatively regulates the osteoclast expression of Spns2 gene, which encodes a transporter for the signaling lipid sphingosine 1-phosphate (S1P). CTR-deficient mice show increased S1P levels, and their skeletal phenotype is normalized by deletion of the S1P receptor S1P3. Finally, pharmacologic treatment with the non-selective S1P receptor agonist FTY720 causes increased bone formation in wildtype, but not in S1P3-deficient mice. This study redefines the role of CT in skeletal biology, confirms that S1P acts as an osteoanabolic molecule in vivo, and provides evidence for a pharmacologically exploitable crosstalk between osteoclasts and osteoblasts. Osteoclasts of wildtype and Calcr-/- C57Bl/6 mice were treated with Calcitonin and compared to the non-treated osteoclasts of wildtype or Calcr-/- mice, respectively.

2014-10-19 | E-GEOD-60761 | biostudies-arrayexpress