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Complementary HLH Susceptibility Factors Converge on CD8 T-cell Hyperactivation [TCR-seq]

ABSTRACT: Complementary HLH Susceptibility Factors Converge on CD8 T-cell Hyperactivation [TCR-seq]

PROVIDER: PRJNA938774 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23620710_1.fastq.gz	Fastqsanger.gz
	SRR23620710_2.fastq.gz	Fastqsanger.gz
	SRR23620711_1.fastq.gz	Fastqsanger.gz
	SRR23620711_2.fastq.gz	Fastqsanger.gz
	SRR23620712_1.fastq.gz	Fastqsanger.gz

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Complementary HLH Susceptibility Factors Converge on CD8 T-cell Hyperactivation

Project description:Complementary HLH Susceptibility Factors Converge on CD8 T-cell Hyperactivation

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Complementary HLH Susceptibility Factors Converge on CD8 T-cell Hyperactivation [bulk RNA-seq]

Project description:Complementary HLH Susceptibility Factors Converge on CD8 T-cell Hyperactivation [bulk RNA-seq]

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Complementary HLH Susceptibility Factors Converge on CD8 T-cell Hyperactivation [TCR-seq]

Project description:To determine the effects of excess IL-18 and perforin deficiency on CD8 T cell clonality toegther and separately under homeostatic conditions. These data support that together perforin deficiency and excess IL-18 promote hyperexpansion of CD8 T cell clones.

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Complementary HLH Susceptibility Factors Converge on CD8 T-cell Hyperactivation

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

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Complementary HLH Susceptibility Factors Converge on CD8 T-cell Hyperactivation [bulk RNA-seq]

Project description:To determine the effects of excess IL-18 and perforin deficiency on CD8 T cells toegther and separately under homeostatic conditions. Mice harboring both excess IL-18 and perforin deficiency (DS) have increased activated (CD44+) CD8 t cells as well as a special CD44low/- CD62L- (DN) population of CD8 T cells. DS mice have CD8 T cells that have specifically upregulated inhibitory receptors Lag3, Havcr2, and Tigit, and the transcription factors Tox and Prdm1. Mice harboring excess IL-18 and partial perforin deficiency (DS-HET) as well as mice with only excess IL-18 (Il18tg) also have these signatures but only in the DN CD8 T cell population. These data support that IL-18 as a potent, independent, and modifiable driver of life-threatening innate nd adaptive hyperinflammation, and support the rationale for an IL-18-driven subclass of hyperinflammation.

2023-09-28 | GSE226125 | GEO

Expression data from C. elegans wild type, hlh-25 mutant and hlh-29 mutant strains

Project description:In Caenorhabditis elegans, the six proteins that make up the REF-1 family are HES homologs that act in both Notch dependent and Notch-independent pathways to regulate embryonic events. To further our understanding of how the REF-1 family works to coordinate post-embryonic cellular events, we performed transcriptome analysis of HLH-25 and HLH-29 mutant strains. Gene expression microarray, including probe preparation, hybridization, fluidics run and chip scan, was performed by Georgia State University DNA/Protein Core Facility. Global gene expression in synchronized young adult populations of VC1220 (hlh-25 mutant) and tm284 (hlh-29 mutant) animals were compared to expression in N2 (wild-type) animals using GeneChip C. elegans Genome Array (Affymetrix). Data collection was carried out using GCOS 1.4 software (Affymetrix). Probe intensity values were normalized to a target value of 500 with normalization factor equal to 1. Data analysis was performed using GeneSpring GX 11 Software (Aglient, Palo Alto,CA).

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