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The histone modification landscape of neonatal CD4+ T cells contributes to decreased T cell receptor signaling

ABSTRACT: The histone modification landscape of neonatal CD4+ T cells contributes to decreased T cell receptor signaling

PROVIDER: PRJNA575695 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10225200.fastq.gz	Fastqsanger.gz
	SRR10225201.fastq.gz	Fastqsanger.gz
	SRR10225161.fastq.gz	Fastqsanger.gz
	SRR10225162.fastq.gz	Fastqsanger.gz
	SRR10225163.fastq.gz	Fastqsanger.gz

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The histone modification landscape of neonatal CD4+ T cells contributes to decreased T cell receptor signaling

Project description:Chromatin immunoprecipitation with massively parallel DNA sequencing (ChIP-seq) was performed to establish the H3K4me3 landscape in neonatal and adult naive CD4+ T cells. As development progressed from neonate to adult, naive CD4+ T cells gained the activating mark H3K4me3 at immunologically important promoter sites. Adult naive CD4+ T cells had enrichment of H3K4me3 at genes important in T cell receptor signaling, which was associated with improved markers of activation and cytokine expression in adult naive CD4+ T cells after engagement of the T cell receptor.

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Project description:Chromatin immunoprecipitation with massively parallel DNA sequencing (ChIP-seq) was then performed to establish the H3K4me3 landscape in neonatal and adult CD14+ monocytes. As development progressed from neonate to adult, monocytes gained the activating mark H3K4me3. The decreased H3K4me3 abundance at immunologically important neonatal monocyte gene promoters correlated with reduced gene expression, providing evidence that neonatal immune cells exist in an epigenetic state that is distinctly different from adults, and that this state contributes to neonatal specific immune responses.

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Project description:Neonates have dampened expression of pro-inflammatory cytokines and difficulty clearing pathogens. This makes them uniquely susceptible to infections, but the factors regulating neonatal-specific immune responses are poorly understood. Epigenetics, including histone modifications, can activate or silence gene transcription by modulating chromatin structure and stability without affecting the DNA sequence itself and are potentially modifiable. Histone modifications are known to regulate immune cell differentiation and function in adults but have not been well studied in neonates.To elucidate the role of histone modifications in neonatal immune function, we performed chromatin immunoprecipitation on mononuclear cells from 45 healthy neonates (gestational ages 23-40 weeks). As gestation approached term, there was increased activating H3K4me3 on the pro-inflammatory IL1B, IL6, IL12B, and TNF cytokine promoters (p?<?0.01) with no change in repressive H3K27me3, suggesting that these promoters in preterm neonates are less open and accessible to transcription factors than in term neonates. Chromatin immunoprecipitation with massively parallel DNA sequencing (ChIP-seq) was then performed to establish the H3K4me3, H3K9me3, H3K27me3, H3K4me1, H3K27ac, and H3K36me3 landscapes in neonatal and adult CD14+ monocytes. As development progressed from neonate to adult, monocytes lost the poised enhancer mark H3K4me1 and gained the activating mark H3K4me3, without a change in additional histone modifications. This decreased H3K4me3 abundance at immunologically important neonatal monocyte gene promoters, including CCR2, CD300C, ILF2, IL1B, and TNF was associated with reduced gene expression.These results provide evidence that neonatal immune cells exist in an epigenetic state that is distinctly different from adults and that this state contributes to neonatal-specific immune responses that leaves them particularly vulnerable to infections.

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