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IL-22 resolves MASLD via enterocyte STAT3 restoration of diet perturbed intestinal homeostasis [scRNA-seq]

ABSTRACT: We found IL22 could reduce intestinal fatty acid transporters expression. We used single cell RNA sequencing (scRNA-seq) to analyze the cell population and gene expression with Fc or IL-22Fc treatment.

ORGANISM(S): Mus musculus

PROVIDER: GSE242927 | GEO | 2024/08/01

REPOSITORIES: GEO

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IL-22 resolves MASLD via enterocyte STAT3 restoration of diet perturbed intestinal homeostasis [16s rDNA-seq]

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IL-22 resolves MASLD via enterocyte STAT3 restoration of diet perturbed intestinal homeostasis

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IL-22 resolves MASLD via enterocyte STAT3 restoration of diet perturbed intestinal homeostasis

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IL-22+ T cells protect intestinal crypts from bacterial invasion and epithelial damage.

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A human STAT3 gain of function variant drives Th17 expansion and IL-22 dependent skin inflammation in a model of psoriasiform dermatitis

Project description:Germline gain-of-function (GOF) variants in STAT3 cause early-onset poly-autoimmunity and immune dysregulation. STAT3 is a pleiotropic transcription factor that affects the induction and regulation of immune responses, with diverse effects on the immune response. Using a mouse model of STAT3 GOF (p.G421R), we observed spontaneous and imiquimod (IMQ)-induced skin inflammation with increased cell-intrinsic local Th17 responses. CD4+ T cells were required and sufficient to drive skin inflammation, and upregulated Il22 expression in expanded clones. However, certain aspects of disease, including epidermal thickness, required the presence of STAT3 GOF in epithelial cells. Treatment with a JAK inhibitor improved skin disease, without affecting local Th17 recruitment and cytokine production. Collectively, these data support a role for a Th17 response and in the development of organ-specific immune dysregulation in STAT3 GOF, and also suggest that the presence of STAT3 GOF in tissues is important for disease and can be targeted with JAK inhibition.

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IL-22 Prevents Epithelial Dysfunction During Citrobacter rodentium-induced Infectious Colitis

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IL-22 Controls Iron-Dependent Nutritional Immunity Against Systemic Bacterial Infections

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