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The impact of pro-inflammatory cytokines on the β-cell regulatory landscape provides insights into the genetics of type 1 diabtes [UMI-4C]

ABSTRACT: The impact of pro-inflammatory cytokines on the β-cell regulatory landscape provides insights into the genetics of type 1 diabtes [UMI-4C]

PROVIDER: PRJNA563891 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10067402_1.fastq.gz	Fastqsanger.gz
	SRR10067402_2.fastq.gz	Fastqsanger.gz
	SRR10067403_1.fastq.gz	Fastqsanger.gz
	SRR10067403_2.fastq.gz	Fastqsanger.gz
	SRR10067404_1.fastq.gz	Fastqsanger.gz

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The impact of pro-inflammatory cytokines on the β-cell regulatory landscape provides insights into the genetics of type 1 diabtes [UMI-4C]

Project description:Early stages of type 1 diabetes (T1D) are characterized by local autoimmune inflammation and progressive loss of insulin-producing pancreatic β cells. We show here that exposure to pro-inflammatory cytokines unmasks a striking plasticity of the β-cell regulatory landscape. We expand the repertoire of human islet regulatory elements by mapping stimulus-responsive enhancers linked to changes in the β-cell transcriptome, proteome and 3D chromatin structure. Our data indicates that the β cell response to cytokines is mediated by the induction of novel regulatory regions as well as the activation of primed regulatory elements pre-bound by islet-specific transcription factors. We found that T1D-associated loci are enriched of the newly mapped cis-regulatory regions and identify T1D-associated variants disrupting cytokine-responsive enhancer activity in human β cells. Our study illustrates how β cells respond to a pro-inflammatory environment and implicate a role for stimulus-response islet enhancers in T1D.

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