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Epithelial-Immune Metabolic Codependency Fuels Inflammatory Disease

ABSTRACT: Epithelial-Immune Metabolic Codependency Fuels Inflammatory Disease

PROVIDER: PRJNA996582 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25342400_1.fastq.gz	Fastqsanger.gz
	SRR25342400_2.fastq.gz	Fastqsanger.gz
	SRR25342401_1.fastq.gz	Fastqsanger.gz
	SRR25342401_2.fastq.gz	Fastqsanger.gz
	SRR25342402_1.fastq.gz	Fastqsanger.gz

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Project description:Inflammatory skin diseases are spurred by unchecked immune-epithelial circuits. However, the specific metabolic factors involved in crosstalk and their impact on the dysregulation of these two cellular components are not well understood. To better decipher the metabolic factors involved in psoriasis, we employed spatial transcriptomics (ST), a ground-breaking technology that precisely maps gene expression from histologically-intact tissue sections. These findings identify therapeutically targetable metabolic vulnerabilities in inflammatory skin disease by unveiling a remarkable coordination of metabolic processes between the epithelial and immune compartments.

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Epithelial-Immune Metabolic Codependency Fuels Inflammatory Disease

Project description:This SuperSeries is composed of the SubSeries listed below.

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Dickkopf1 fuels inflammatory cytokine responses

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Project description:Many human diseases, including cancer, share an inflammatory component but the molecular underpinnings remain incompletely understood. We report that physiological and pathological Dickkopf1 (DKK1) activity fuels inflammatory cytokine responses in cell models, mice and humans. DKK1 maintains the elevated inflammatory tone of cancer cells and is required for mounting cytokine responses following ligation of toll-like and cytokine receptors. DKK1-controlled inflammation derives from cell-autonomous mechanisms, which involve SOCS3-restricted, nuclear RelA (p65) activity. We translate these findings to humans by showing that genetic DKK1 variants are linked to elevated cytokine production across healthy populations. Finally, we find that genetic deletion of DKK1 but not pharmacological neutralization of soluble DKK1 ameliorates inflammation and disease trajectories in a mouse model of endotoxemia. Collectively, our study identifies a cell-autonomous function of DKK1 in the control of the inflammatory response, which is conserved between malignant and non-malignant cells and may be exploited therapeutically in the future.

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