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Prioritization of autoimmune disease-associated genetic variants that perturb regulatory element activity in T cells [MPRA]

ABSTRACT: Prioritization of autoimmune disease-associated genetic variants that perturb regulatory element activity in T cells [MPRA]

PROVIDER: PRJNA810856 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18158550_1.fastq.gz	Fastqsanger.gz
	SRR18158550_2.fastq.gz	Fastqsanger.gz
	SRR18158551.fastq.gz	Fastqsanger.gz
	SRR18158552.fastq.gz	Fastqsanger.gz
	SRR18158553.fastq.gz	Fastqsanger.gz

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Prioritization of autoimmune disease-associated genetic variants that perturb regulatory element activity in T cells

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Project description:Determining causal variants for autoimmune disease is an enormous challenge - 90% of autoimmune disease-associated variants are non-coding and there are often 10s-100s are in tight linkage disequilibrium with the causal variant(s), making identification of the true causal variants difficult. Using massively parallel reporter assays in a T cell line, we prioritized variants that enriched highly for likely causal variants according to statistical fine-mapping. We followed up on one of the prioritized variants, rs72928038 in the BACH2 locus, which had a high effect size, finding that it regulates Bach2 expression in a human T cell line. We created mice containing a small deletion over this non-coding variant, and have tested mutant vs. WT antigen-specific T cells for their responses during acute viral infection. In the context of rs72928038-deleted mice (termed Bach218del), we found an increase in effector T cell differentiation, which highlights a potential role for rs72928038 in modulating effector T cell differentiation in the context of autoimmune disease.

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