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FOXP3 exon 2 controls Treg stability and autoimmunity [ChIP-seq]

ABSTRACT: FOXP3 exon 2 controls Treg stability and autoimmunity [ChIP-seq]

PROVIDER: PRJNA819105 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18458261.fastq.gz	Fastqsanger.gz
	SRR18458262.fastq.gz	Fastqsanger.gz
	SRR18458263.fastq.gz	Fastqsanger.gz
	SRR18458264.fastq.gz	Fastqsanger.gz
	SRR18458265.fastq.gz	Fastqsanger.gz

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FOXP3 exon 2 controls Treg stability and autoimmunity

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Project description:Differing from the mouse Foxp3 gene that encodes only one protein product, human FOXP3 encodes two major isoforms through alternative splicing – a longer isoform (FOXP3 FL) containing all the coding exons and the other shorter isoform lacking the amino acids encoded by exon 2 (FOXP3 ΔE2). The two isoforms are naturally expressed in humans yet their differences in controlling regulatory T cell phenotype and functionality remains unclear. Here we show that patients expressing only the shorter isoform failed to maintain self-tolerance and developed IPEX syndrome. Mice with Foxp3 exon 2 deletion developed excessive TFH and GC B cell responses and systemic autoimmune disease with anti-dsDNA and anti-nuclear autoantibody production and immune-complex glomerulonephritis. Regulatory T cells expressing FOXP3 ΔE2 were unstable and sufficient to induce autoimmunity when transferred into Tcrb-deficient mice. Mechanistically, FOXP3 ΔE2 isoform allows increased expression of selected cytokines but decreased expression of a set of Foxp3 positive regulators without altered binding to these gene loci. We demonstrate that exon 2 of FOXP3 is required to maintain Treg stability and immune homeostasis.

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