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IRF5 genetic risk variants drive myeloid-specific IRF5 hyper-activation and pre-symptomatic SLE

ABSTRACT: IRF5 genetic risk variants drive myeloid-specific IRF5 hyper-activation and pre-symptomatic SLE

PROVIDER: PRJNA564499 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10084441.fastq.gz	Fastqsanger.gz
	SRR10084442.fastq.gz	Fastqsanger.gz
	SRR10084443.fastq.gz	Fastqsanger.gz
	SRR10084444.fastq.gz	Fastqsanger.gz
	SRR10084445.fastq.gz	Fastqsanger.gz

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IRF5 genetic risk variants drive myeloid-specific IRF5 hyper-activation and pre-symptomatic SLE

Project description:The IRF5-SLE risk haplotype is associated with SLE disease severity. We hypothesized that neutrophils from healthy risk donors would carry a pathogenic gene signature compared to non-risk donors. To compare basal neutrophil gene signature between risk and non-risk healthy individuals, fresh whole blood was collected from healthy donors, and granulocytes were extracted from the remaining pellet following Ficoll purification. RNA-seq libraries were prepared from globin-reduced RNA extracted from the granulocytes using the Qiagen RNA preparation kit.

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Transcriptome analysis of peripheral blood from Lyn-deficient mouse SLE model lacking Ifnar1 or Irf5

Project description:To clarify the role of interferon regulatory factor 5 (IRF5) other than inducing type I interferons (IFNs) in the pathogenesis of systemic lupus erythematosus (SLE), we performed transcriptome analysis of peripheral blood from Lyn-deficient mice with concomitant Ifnar1 or Irf5 deficiency. The results of gene set enrichment analysis (GSEA) suggest that IRF5 is involved in the induction of not only IFN-inducible genes (ISGs) but also oxidative phosphorylation (OXPHOS)-related genes in the SLE pathogenesis.

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IRF5 genetic risk variants drive myeloid-specific IRF5 hyperactivation and presymptomatic SLE.

Project description:Genetic variants within or near the interferon regulatory factor 5 (IRF5) locus associate with systemic lupus erythematosus (SLE) across ancestral groups. The major IRF5-SLE risk haplotype is common across populations, yet immune functions for the risk haplotype are undefined. We characterized the global immune phenotype of healthy donors homozygous for the major risk and nonrisk haplotypes and identified cell lineage-specific alterations that mimic presymptomatic SLE. Contrary to previous studies in B lymphoblastoid cell lines and SLE immune cells, IRF5 genetic variants had little effect on IRF5 protein levels in healthy donors. Instead, we detected basal IRF5 hyperactivation in the myeloid compartment of risk donors that drives the SLE immune phenotype. Risk donors were anti-nuclear antibody positive with anti-Ro and -MPO specificity, had increased circulating plasma cells and plasmacytoid dendritic cells, and had enhanced spontaneous NETosis. The IRF5-SLE immune phenotype was conserved over time and probed mechanistically by ex vivo coculture, indicating that risk neutrophils are drivers of the global immune phenotype. RNA-Seq of risk neutrophils revealed increased IRF5 transcript expression, IFN pathway enrichment, and decreased expression of ROS pathway genes. Altogether, the data support that individuals carrying the IRF5-SLE risk haplotype are more susceptible to environmental/stochastic influences that trigger chronic immune activation, predisposing to the development of clinical SLE.

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Genome-wide profiling of target genes for the systemic lupus erythematosus-associated transcription factors IRF5 and STAT4

Project description:IRF5 and STAT4 are strongly associated with human systemic lupus erythematosus (SLE). By performing chromatin immunoprecipitation-sequencing (ChIP-Seq) in human peripheral blood mononuclear cells (PBMCs), we identified more than 7000 target genes for IRF5 and STAT4 in stimulated PBMCs. Contrarily, without stimulation IRF5 seemed to be inactive, and STAT4 only showed low levels of transcriptional regulatory activity. Target genes of IRF5 and STAT4 were identified in human PBMCs with or without stimulation using ChIP-Seq.

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Expression analysis of Reh cells after transfection with constitutively active variants of IRF5 (IRF5-4D) and/or constitutively active IKKÎ²(EE)

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Genome-wide maps of chromatin state of IRF5+/+ and IRF5-/- CD4+ mouse T cells

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Expression analysis of Reh cells after transfection with constitutively active variants of IRF5 (IRF5-4D) and/or constitutively active IKKβ(EE)

Project description:Genome-wide gene expression analysis of Reh cells following transfection with constitutively active IRF5-4D, constitutively active IKKβ(EE), or both in combination.

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Transcriptome analysis of peripheral blood from Lyn-deficient mouse SLE model lacking Ifnar1 or Irf5

Project description:Transcriptome analysis of peripheral blood from Lyn-deficient mouse SLE model lacking Ifnar1 or Irf5

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