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Translational implications of Th17-skewed inflammation due to genetic deficiency of a cadherin stress sensor II

ABSTRACT: Translational implications of Th17-skewed inflammation due to genetic deficiency of a cadherin stress sensor II

PROVIDER: PRJNA781568 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16975110_1.fastq.gz	Fastqsanger.gz
	SRR16975110_2.fastq.gz	Fastqsanger.gz
	SRR16975114_1.fastq.gz	Fastqsanger.gz
	SRR16975114_2.fastq.gz	Fastqsanger.gz
	SRR16975117_1.fastq.gz	Fastqsanger.gz

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Translational implications of Th17-skewed inflammation due to genetic deficiency of a cadherin stress sensor III

Project description:Translational implications of Th17-skewed inflammation due to genetic deficiency of a cadherin stress sensor III

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Translational implications of Th17-skewed inflammation due to genetic deficiency of a cadherin stress sensor I

Project description:Translational implications of Th17-skewed inflammation due to genetic deficiency of a cadherin stress sensor I

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Translational implications of Th17-skewed inflammation due to genetic deficiency of a cadherin stress sensor I

Project description:Desmoglein 1 (Dsg1) is a cadherin restricted to stratified tissues of terrestrial vertebrates, which serve as essential physical and immune barriers. Dsg1 loss-of-function mutations in humans result in skin lesions, multiple allergies, and isolated patient keratinocytes exhibit increased pro-allergic cytokine expression. However, the mechanism by which genetic deficiency of Dsg1 causes chronic inflammation is unknown. To determine the systemic response to Dsg1 loss, we deleted the three tandem Dsg1 genes in mice. Whole transcriptome analysis of embryonic Dsg1-/- skin showed a delay in expression of adhesion/differentiation/keratinization genes at E17.5, a subset of which recovered or increased by E18.5. Comparing epidermal transcriptomes from Dsg1-deficient mice and humans revealed a shared IL-17-skewed inflammatory signature. Although the impaired intercellular adhesion observed in Dsg1-/- mice resembles that resulting from anti-Dsg1 pemphigus foliaceus antibodies, pemphigus skin lesions exhibit a weaker IL-17 signature. Consistent with the clinical importance of these findings, treatment of two Dsg1-deficient patients with an IL-12/IL-23 antagonist originally developed for psoriasis resulted in improvement of skin lesions. Thus, beyond impairing the physical barrier, loss of Dsg1 function through gene mutation results in a psoriatic-like inflammatory signature before birth and treatment with a targeted therapy significantly improved skin lesions in patients.

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Translational implications of Th17-skewed inflammation due to genetic deficiency of a cadherin stress sensor II

2021-11-25 | GSE189095 | GEO

Translational implications of Th17-skewed inflammation due to genetic deficiency of a cadherin stress sensor III

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Translational implications of Th17-skewed inflammation due to genetic deficiency of a cadherin stress sensor.

Project description:Desmoglein 1 (Dsg1) is a cadherin restricted to stratified tissues of terrestrial vertebrates, which serve as essential physical and immune barriers. Dsg1 loss-of-function mutations in humans result in skin lesions and multiple allergies, and isolated patient keratinocytes exhibit increased proallergic cytokine expression. However, the mechanism by which genetic deficiency of Dsg1 causes chronic inflammation is unknown. To determine the systemic response to Dsg1 loss, we deleted the 3 tandem Dsg1 genes in mice. Whole transcriptome analysis of embryonic Dsg1-/- skin showed a delay in expression of adhesion/differentiation/keratinization genes at E17.5, a subset of which recovered or increased by E18.5. Comparing epidermal transcriptomes from Dsg1-deficient mice and humans revealed a shared IL-17-skewed inflammatory signature. Although the impaired intercellular adhesion observed in Dsg1-/- mice resembles that resulting from anti-Dsg1 pemphigus foliaceus antibodies, pemphigus skin lesions exhibit a weaker IL-17 signature. Consistent with the clinical importance of these findings, treatment of 2 Dsg1-deficient patients with an IL-12/IL-23 antagonist originally developed for psoriasis resulted in improvement of skin lesions. Thus, beyond impairing the physical barrier, loss of Dsg1 function through gene mutation results in a psoriatic-like inflammatory signature before birth, and treatment with a targeted therapy significantly improved skin lesions in patients.

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Characterization of microRNA signature in activated CD4+ T, polyclonal Th17 (Th17 poly), OVA-specific Th17 (Th17 Ag-sp) cell skewed cultures

Project description:To determine specific miRNAs for Th17 cells, we performed comparative miRNA screening of activated CD4+ T, polyclonal Th17 (Th17 poly) and OVA-specific Th17 (Th17 Ag-sp) cell skewed cultures or Th17 Ag-sp sorted cells. The expression of miRNAs analyzed by microarray revealed 27 miRNAs exclusively expressed in culture or sorted Th17 Ag-sp cell subset.

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Characterization of microRNA signature in activated CD4+ T, polyclonal Th17 (Th17 poly), OVA-specific Th17 (Th17 Ag-sp) cell skewed cultures

Project description:Characterization of microRNA signature in activated CD4+ T, polyclonal Th17 (Th17 poly), OVA-specific Th17 (Th17 Ag-sp) cell skewed cultures

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Differentially expressed microRNAs in antigen-specific Th17 cell cultures from WT and CD69KO mice

Project description:To explore miRNA signature in T cells during moderate (wild type BALB/c) and severe (cd69-/- in BALB/c background) EAM development, we performed microarray experiments with OVA-specific Th17 (Th17 Ag-sp) cell skewed cultures. The comparison of miRNA profiles from Th17 Ag-sp subsets of cd69-/- and wild type mice, with severe and mild EAM respectively, revealed a number of deregulated miRNAs.

2021-01-01 | GSE109993 | GEO

CIP2A negatively regulates Th17 differentiation

Project description:Interleukin 17 (IL-17) producing T helper 17 (Th17) cells are critical drivers of pathogenesis in a variety of autoimmune and inflammatory diseases. Strategies to mitigate excessive Th17 response thus remain an attractive target for immunotherapies. Here we report that Cancerous Inhibitor of Protein Phosphatase 2A (CIP2A) regulates IL-17 production by Th17 cells in human and mouse. Using CIP2A knock-out (KO) mice and siRNA-mediated CIP2A silencing in human primary CD4+ T cells, we demonstrated that CIP2A silencing results in a significant increase in IL-17 production. Interestingly, CIP2A deficient Th17 cells were characterized by increased strength and duration of STAT3 (Y705) phosphorylation. Genome-wide gene expression profile as well as the p-STAT3 (Y705) interactome of CIP2A deficient Th17 cells identified that CIP2A regulates the strength of the interaction between Acylglycerol kinase (AGK) and STAT3, and thereby, modulates STAT3 phosphorylation as well as expression of IL-17 in Th17 cells. Our results uncover the physiological function of CIP2A in Th17 cells and provides new opportunities for therapeutic intervention in Th17 cell mediated diseases.

2020-05-26 | PXD010612 | Pride

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