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The transcription factor Fosl2 controls systemic autoimmunity by repressing FoxP3 during T cell development

ABSTRACT: The transcription factor Fosl2 controls systemic autoimmunity by repressing FoxP3 during T cell development

PROVIDER: PRJNA547589 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9211590_1.fastq.gz	Fastqsanger.gz
	SRR9211590_2.fastq.gz	Fastqsanger.gz
	SRR9211591_1.fastq.gz	Fastqsanger.gz
	SRR9211591_2.fastq.gz	Fastqsanger.gz
	SRR9211583_1.fastq.gz	Fastqsanger.gz

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The transcription factor Fosl2 controls systemic autoimmunity by repressing FoxP3 during T cell development

Project description:Purpose: We aimed to charaterise the transfriptional effects of Fosl2 in T cells Methods: We used wt, Fosl2 overexpressing (Fosl2tg) and Fosl2 knock-out (Fosl2ko) CD4+ naive T cells that we stimulated for 24 hours with anti-CD3 and anti-CD28. RNA-was extracted and sequenced using Results: We identified a set of genes whose expression is regulated by Fosl2 in T cells, including Foxp3.

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

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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FOXP3 exon 2 controls Treg stability and autoimmunity

Project description:FOXP3 exon 2 controls Treg stability and autoimmunity

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

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

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Effect of NIK overexpression on Foxp3+CD4+ and Foxp3-CD4+ T cell subsets [Illumina]

Project description:We previously found that NF-kB inducing kinase (NIK) overexpression in T cells via CD4 promoter driven transgene induction caused lethal autoimmunity in mice. Autoimmunity was associated with increased conventional T cell effector function and decreased regulatory T cell (Foxp3+CD4+) suppression. The goal in this study was to elucidate global transcriptional changes in Foxp3+CD4+ and Foxp3-CD4+ T cells intrinsically caused by chronic NIK overexpression in these cell types.

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Mapping interactome networks of FOSL1 and FOSL2 in human Th17 cells

Project description:The differentiation of Th17 cells is controlled by a complex network of transcription factors (TFs), including FOS and JUN proteins of the AP-1 family. The FOS-like proteins, FOSL1 and FOSL2 have recently been reported to control Th17 responses. The molecular mechanisms dictating their roles, however, are unclear. Moreover, although the functions of AP-1 TFs are largely governed by their protein-protein interactions, these are also poorly characterized in this milieu. Using affinity purification in combination with mass-spectrometry we established the first interactomes of FOSL1 and FOSL2 in human Th17 cells. In addition to their known interactions with JUN proteins, our analysis identified several novel binding partners of FOSL factors. Gene ontology analysis revealed RNA binding was enriched as the major functionality for FOSL1 and FOSL2 associated proteins, thereby suggesting possible mechanistic links that have not been studied before. Intriguingly, 29 interactors were found to be shared between FOSL1 and FOSL2, which included crucial regulators of Th17-fate. These findings, including unique and shared interactions, were validated using parallel reaction monitoring targeted mass-spectrometry (PRM-MS), with additional measurements with other laboratory methods. Overall, this study provides key insights into interaction-based signalling mechanisms of FOSL1 and FOSL2, which potentially control Th17 cell-development and associated pathologies.

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Effect of NIK overexpression on Foxp3+CD4+ and Foxp3-CD4+ T cell subsets [Affymetrix]

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