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

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

PROVIDER: PRJNA938773 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23620831.fastq.gz	Fastqsanger.gz
	SRR23620832.fastq.gz	Fastqsanger.gz
	SRR23620833.fastq.gz	Fastqsanger.gz
	SRR23620834.fastq.gz	Fastqsanger.gz
	SRR23620835.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

| PRJNA938772 | ENA

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

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

| PRJNA938774 | ENA

Complementary HLH Susceptibility Factors Converge on CD8 T-cell Hyperactivation

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

2023-09-28 | GSE226126 | GEO

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.

2023-09-28 | GSE226124 | GEO

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

A conserved cysteine-based redox mechanism sustains TFEB/HLH-30 activity under persistent stress

Project description:Mammalian TFEB and TFE3, as well as their ortholog in C. elegans HLH-30, play an important role in mediating cellular response to a variety of stress conditions, including nutrient deprivation, oxidative stress and pathogen infection. In this study we identify a novel mechanism of TFEB/HLH-30 regulation through a cysteine-mediated redox switch. Under stress conditions, TFEB-C212 undergoes oxidation, allowing the formation of intermolecular disulfide bonds that result in TFEB oligomerization. TFEB oligomers display increased resistance to mTORC1-mediated inactivation and are more stable under prolonged stress conditions. Mutation of the only cysteine residue present in HLH-30 (C284) significantly reduced its activity, resulting in developmental defects and increased pathogen susceptibility. Therefore, cysteine oxidation represents a new type of TFEB post-translational modification that functions as a molecular switch to link changes in redox balance with expression of TFEB/HLH-30 target genes.

2021-01-22 | PXD022258 | Pride

Targeted sequencing of 12 genes in patients with HLH

Project description:Hemophagocytic lymphohistiocytosis (HLH) is a rapid-onset, potentially fatal hyperinflammatory syndrome. A prompt molecular diagnosis is crucial for appropriate clinical management. Here, we validated and prospectively evaluated a targeted high-throughput sequencing approach for HLH diagnostics. We have carried out high-throughput sequencing of 12 genes linked to HLH in 58 HLH patients. We achieved a diagnosis in 22 out of 58 patients (38%). Genetically undiagnosed HLH patients had a later age at onset and manifested higher frequencies of known secondary HLH triggers. Rare, putatively pathogenic monoallelic variants were identified in 9 patients. Almost all cases with reduced natural killer (NK) cell function received a diagnosis, but the majority of the prospective cases remain genetically unexplained, highlighting genetic heterogeneity and environmental impact within HLH. A complete understanding of the genetic susceptibility to HLH thus requires further in-depth investigations, including genome sequencing and detailed immunological characterization.

| EGAS00001001605 | EGA

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).

2016-07-03 | E-GEOD-65417 | biostudies-arrayexpress

Prenatal inflammation remodels lung immunity and function by programming ILC2 hyperactivation

Project description:We examined how prenatal inflammation shapes tissue function and immunity in the lung by reprogramming tissue-resident immune cells from early development. Maternal, but not fetal, type I interferon-mediated inflammation provoked expansion and hyperactivation of group 2 innate lymphoid cells (ILC2s) seeding the developing lung. Hyperactivated ILC2s produced increased IL-5 and IL-13, were associated with acute Th2 bias, decreased Tregs, and persistent lung eosinophilia into adulthood. ILC2 hyperactivation was recapitulated by adoptive transfer of a fetal liver precursor following prenatal inflammation, indicative of developmental programming at the fetal progenitor level. Reprogrammed ILC2 hyperactivation and subsequent lung immune remodeling, including persistent eosinophilia, was associated with worsened histopathology and increased airway dysfunction equivalent to papain exposure, indicating increased asthma susceptibility in offspring. Our data elucidate a potential mechanism by which early-life inflammation results in increased asthma susceptibility, driven by hyperactivated ILC2s that drive persistent changes to lung immunity during perinatal development.

2024-06-24 | GSE268129 | GEO

mRNA-seq of wild-type(N2), hlh-11 knock-out(KO) and hlh-11 over-expression(OE) worms

Project description:Purpose: Comparing the transcriptome of wild-type(N2), hlh-11 knock-out and hlh-11 over-expression worms to identify genes with differential expression. Methods: For each condition, two replicates were examined. For each sample, approximately 2,000 synchronized young adult worms were collected and resuspended in TRIzon Reagent (CW0580, CWBIO). Total RNA was isolated by chloroform extraction, followed by isopropanol precipitation. Sequencing was performed using HiSeq2500. The clean reads were aligned to WBcel235 genomes with TopHat2. Gene differential expression was analyzed using DEseq2. A threshold of p < 0.05 was set to determine differentially expressed genes. Induction (KO_up or OE_up) or suppression (KO_down or OE_down) of genes were obtained through comparing gene expressions in hlh-11 KO or OE worms to wild-type N2. Results: >86% reads were uniquely mapped. 2637 genes were significantly up regulated and 2845 genes were significantly down regulated in hlh-11 knock-out worms compared to wild-type. 107 genes were significantly up regulated and 237 genes were significantly down regulated in hlh-11 over-expression worms compared to wild-type. Conclusions: This study revealed the genes transcriptionally regulated by hlh-11.

2019-11-23 | GSE140866 | GEO

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