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Epigenome profiling reveals significant DNA demethylation of interferon signature genes in lupus neutrophils

ABSTRACT: We identified genome-wide DNA methylation patterns within neutrophils and low-density granulocytes of Lupus patients and demographically matched controls

ORGANISM(S): Homo sapiens

PROVIDER: GSE65097 | GEO | 2015/01/21

SECONDARY ACCESSION(S): PRJNA272992

REPOSITORIES: GEO

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Epigenome profiling reveals significant DNA demethylation of interferon signature genes in lupus neutrophils

Project description:We identified genome-wide DNA methylation patterns within neutrophils and low-density granulocytes of Lupus patients and demographically matched controls Comparison of 15 Lupus patients vs 15 age-, sex-, and ethnicity-matched controls using the Illumina HumanMethylation 450 beadchip array

2015-01-21 | E-GEOD-65097 | biostudies-arrayexpress

Epigenome profiling reveals significant DNA demethylation of interferon signature genes in lupus neutrophils.

Project description: Not available

| S-EPMC4363276 | biostudies-literature

Human lupus netting neutrophils induce endothelial damage, infiltrate tissues and expose immunostimulatory molecules

Project description:Our group has proposed that low-density granulocytes (LDGs) play an important role in lupus pathogenesis, as they can damage endothelial cells and synthesize increased levels of proinflammatory cytokines and type I interferons. LDGs have a heightened capacity to synthesize neutrophil extracellular traps (NETs). NETs from LDGs display increased levels of bactericidal and immunostimulatory proteins, such as the cathelicidin LL37 and externalize double-stranded DNA (dsDNA). Lupus netting LDGs have increased capacity to kill endothelial cells and expose IL-17. Through NETosis, lupus neutrophils stimulate plasmacytoid DCs to synthesize IFN-?. Our results further expand the potential pathogenic role of aberrant lupus neutrophils through a NET-mediated effect. We used microarrays to analyze the gene expression of neutrophils in healthy and lupus patients, and of low-density granulocytes in lupus patients. Human neutrophils and LDGs were isolated from PBMCs. RNA from healthy neutrophils, lupus neutrophils and lupus LDGs was extracted and processed for hybridization on Affymetrix microarrays.

2011-06-22 | E-GEOD-26975 | biostudies-arrayexpress

Human lupus netting neutrophils induce endothelial damage, infiltrate tissues and expose immunostimulatory molecules

Project description:Our group has proposed that low-density granulocytes (LDGs) play an important role in lupus pathogenesis, as they can damage endothelial cells and synthesize increased levels of proinflammatory cytokines and type I interferons. LDGs have a heightened capacity to synthesize neutrophil extracellular traps (NETs). NETs from LDGs display increased levels of bactericidal and immunostimulatory proteins, such as the cathelicidin LL37 and externalize double-stranded DNA (dsDNA). Lupus netting LDGs have increased capacity to kill endothelial cells and expose IL-17. Through NETosis, lupus neutrophils stimulate plasmacytoid DCs to synthesize IFN-α. Our results further expand the potential pathogenic role of aberrant lupus neutrophils through a NET-mediated effect. We used microarrays to analyze the gene expression of neutrophils in healthy and lupus patients, and of low-density granulocytes in lupus patients.

2011-06-22 | GSE26975 | GEO

Oxidized mitochondrial nucleoids released by neutrophils drive type I Interferon production in human lupus

Project description:Autoantibodies against nucleic acids and excessive type I Interferon (IFN) are hallmarks of human Systemic Lupus Erythematosus (SLE). We previously reported that SLE neutrophils, exposed to TLR7-agonist autoantibodies, release interferogenic DNA, which we now demonstrate to be of mitochondrial origin. We further show that healthy human neutrophils do not complete mitophagy upon induction of mitochondrial damage. Rather, they extrude mitochondrial components, including DNA (mtDNA), devoid of oxidized residues. When MtDNA undergoes oxidation, it is directly routed to lysosomes for degradation. This rerouting requires dissociation from the transcription factor TFAM, a dual high mobility group (HMG) protein involved in maintenance and compaction of the mitochondrial genome into nucleoids. Exposure of SLE neutrophils, or healthy IFNprimed neutrophils, to anti-RNP autoantibodies blocks TFAM phosphorylation, a necessary step for nucleoid dissociation. Consequently, oxidized nucleoids accumulate within mitochondria and are eventually extruded as potent interferogenic complexes. In support of the in vivo relevance of this phenomenon, mitochondrial retention of oxidized nucleoids is a feature of SLE blood neutrophils, and autoantibodies against oxidized mtDNA are present in a fraction of patients. This pathway represents a novel therapeutic target in human SLE. 4 samples, no replicates, 2 controls. 2 samples are Neutrophils cultured with and without CCCP (control). 2 samples are Monocytes cultured with and without CCCP (control).

2016-04-07 | E-GEOD-78243 | biostudies-arrayexpress

Transcriptomic data for splenic neutrophils isolated from female NZBWF1/J lupus mice

Project description:Recent literature has shown that neutrophils exert significant influence on the course of disease progression in lupus, but there is currently controversy in the lupus field regarding a) whether neutrophils are predominantly protective or deleterious toward the propagation of auto-reactivity, b) the specific mechanism of neutrophil influence on adaptive immune dysregulation, and c) identity and origin of functionally abnormal neutrophil subsets in lupus. Here we used RNA sequencing of splenic neutrophils isolated from a murine lupus model (NZB/W) to characterize changes in the transcriptional program of neutrophils over the course of lupus progression. We find that the transcription of immunologically relevant genes change over the course of disease, and that lupus neutrophils early in disease show enrichment for transcripts associated with neutrophil precursors. These data provide the first detailed profile of the splenic neutrophil transcriptional program changes during the progression of lupus.

2017-05-10 | GSE97439 | GEO

Oxidized mitochondrial nucleoids released by neutrophils drive type I Interferon production in human lupus

2016-04-07 | GSE78243 | GEO

Transcriptional profiles of pediatric SLE neutrophils and Healthy neutrophils cultured with SLE sera or Interferon

Project description:Mature neutrophis were freshly isolated from blood of pediatric systemic lupus erythematosus (SLE) patients and healthy donors. Illumina microarray was used to assess transcriptional changes between SLE group and Control group. To uderstand further the gene expression difference between SLE and healthy neutrofils, neutrophils from healthy donors were cultured with autologous sera, SLE sera or Interferon and microarray data was used to compare with fresh SLE neutrophils. (Expt 1) Neutrophils from 21 SLE samples (19 patients) and 12 healthy donors were isolated, and extracted RNAs were used generate microarray data. (Expt 2) Neutrophils isolated from 2 healthy children (not used in the first experiment) were cultured with autologous sera (control), Interferon alpha (100U and 1000U), and 4 SLE sera and 6 SLE sera for 6 hours and RNAs were extract for microarray experiment.

2011-03-10 | E-GEOD-27427 | biostudies-arrayexpress

Transcriptional profiles of pediatric SLE neutrophils and Healthy neutrophils cultured with SLE sera or Interferon

2011-03-10 | GSE27427 | GEO

Expression profile of mature normal PB neutrophils

Project description:The transcriptional patterns of mature normal PB neutrophils (granulocytes) was examined and used as a control against which the transcriptional programs of cultured granulocytes and granulocytic cells lines can be compared. Keywords: Peripheral blood neutrophils

2007-06-06 | GSE6792 | GEO

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