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Epigenomes and Transcriptomes of human monocytes from Hyper IgD Syndrome (HIDS) patients

ABSTRACT: Epigenomes and Transcriptomes of human monocytes from Hyper IgD Syndrome (HIDS) patients

PROVIDER: PRJNA412227 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6077560_1.fastq.gz	Fastqsanger.gz
	SRR6077560_2.fastq.gz	Fastqsanger.gz
	SRR6077570.fastq.gz	Fastqsanger.gz
	SRR6077580.fastq.gz	Fastqsanger.gz
	SRR6077561_1.fastq.gz	Fastqsanger.gz

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Epigenomes and Transcriptomes of human monocytes from Hyper IgD Syndrome (HIDS) patients

Project description:Innate immune memory, also refered to as trained immunity (TRIM) is the phenomenon whereby innate immune cells such as monocytes or macrophages undergo functional reprogramming after exposure to microbial components. In this study we performed epigenomic and transcriptomic analysis of HIDS (Hyper IgD Syndrome) patients at baseline, and after 24 hours culture in media (RPMI only) or media + 10ng/mL LPS. HIDS is associated with the accumulation of mevalonate, a monocyte trainer.

2018-01-08 | GSE104282 | GEO

Multi-OMICS data of a Hyper IgD Syndrome family

Project description:The aim of this study was to understand why two siblings carrying both the same homozygous causal mutation for the auto-inflammatory disease hyper IgD show opposite phenotypes, i.e. the first being asymptomatic, the second presenting all classical characteristics of the disease. As compared to studies of a single omics type, the multi-omics approach becomes a method of choice to resolve complex traits. Here we combined exome, proteome and transcriptome analysis in the two siblings and identified a single gene - STAT1 - harboring a rare missense variant and showing mRNA and protein abundances significantly more important in the symptomatic than the asymptomatic sister. This mutation was shown to be a gain of function mutation involved in an increased activation of the JAK/STAT pathway which is known to play a critical role in inflammatory diseases and for which specific bio-therapies exist. Pathway analysis based on information from differentially expressed transcripts and proteins confirmed the central role of STAT1 in the proposed regulatory network leading to an increased inflammatory phenotype in the symptomatic sibling. In addition, we provide a proteogenomics analysis pipeline that takes advantage of subject-specific genomic and transcriptomic information to improve protein identifications. In conclusion, this study demonstrates the power of a multi-omics approach to uncover potentially clinically actionable targets for a personalized therapy.

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Nummular keratopathy in a patient with Hyper-IgD Syndrome.

Project description:PurposeTo report a case of recurrent nummular keratitis in a pediatric patient with Hyperimmunoglobulinemia D syndrome.MethodsA retrospective chart review.ResultsA 14-year-old boy with Hyperimmunoglobulinemia D syndrome (HIDS) presented with photophobia and ocular irritation concomitant with disease exacerbation. He was found on exam to have significant nummular keratitis, which responded to a short course of topical steroids. Despite acute response to local immunosuppression, the patient had several recurrent attacks and eventually developed a large corneal scar and decreased vision. After initiation of infliximab therapy his ocular sequelae improved dramatically and his vision returned to 20/20.ConclusionOne possible form of end-organ damage associated with HIDS is vision threatening nummular keratopathy.

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Microarray analysis of splenic naive IgD+CD27- and IgD+CD27+ B cell subsets cells from adult humans

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