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Epithelial retinoic acid receptor beta regulates serum amyloid A expression and vitamin A-dependent intestinal immunity

ABSTRACT: Retinoic acid receptor beta regulates intestinal immune transcriptional programs

ORGANISM(S): Mus musculus

PROVIDER: GSE122471 | GEO | 2019/02/28

REPOSITORIES: GEO

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Epithelial retinoic acid receptor β regulates serum amyloid A expression and vitamin A-dependent intestinal immunity.

Project description:Vitamin A is a dietary component that is essential for the development of intestinal immunity. Vitamin A is absorbed and converted to its bioactive derivatives retinol and retinoic acid by the intestinal epithelium, yet little is known about how epithelial cells regulate vitamin A-dependent intestinal immunity. Here we show that epithelial cell expression of the transcription factor retinoic acid receptor β (RARβ) is essential for vitamin A-dependent intestinal immunity. Epithelial RARβ activated vitamin A-dependent expression of serum amyloid A (SAA) proteins by binding directly to Saa promoters. In accordance with the known role of SAAs in regulating Th17 cell effector function, epithelial RARβ promoted IL-17 production by intestinal Th17 cells. More broadly, epithelial RARβ was required for the development of key vitamin A-dependent adaptive immune responses, including CD4+ T-cell homing to the intestine and the development of IgA-producing intestinal B cells. Our findings provide insight into how the intestinal epithelium senses dietary vitamin A status to regulate adaptive immunity, and highlight the role of epithelial cells in regulating intestinal immunity in response to diet.

| S-EPMC6561173 | biostudies-literature

Epithelial retinoic acid receptor beta regulates serum amyloid A expression and vitamin A-dependent intestinal immunity

Project description:Epithelial retinoic acid receptor beta regulates serum amyloid A expression and vitamin A-dependent intestinal immunity

| PRJNA505318 | ENA

Effect of Exogenous Retinoic Acid on human iPSCs derived intestinal organoids

Project description:Retinoic acid promotes the in vitro growth, patterning and improves the cellular composition of human pluripotent stem-cell-derived intestinal organoids

2022-09-02 | GSE212333 | GEO

Exit from HSC dormancy is controlled via vitamin A/retinoic acid (II)

Project description:Identification of the role of retinoic acid on the activation of the dHSCs

2017-05-15 | GSE87807 | GEO

Exit from HSC dormancy is controlled via vitamin A/retinoic acid (I)

Project description:Identification of the role of retinoic acid on the activation of the dHSCs

2017-05-15 | GSE87763 | GEO

Effect of Exogenous Retinoic Acid on human iPSCs derived intestinal organoids

Project description:Effect of Exogenous Retinoic Acid on human iPSCs derived intestinal organoids

| PRJNA875061 | ENA

Retinoic acid-induced Transcriptional Signature in Mouse Fibroblast cells

Project description:During intestinal wound healing process, wound-associated epithelial (WAE) cells are differentiated from neighboring crypts and migrate to cover the wound bed. We found that WAE cells can produce retinoic acid via aldh1a3 and secrete it into wound bed. WAE cells and fibroblasts are highly colocalized in wound bed, suggesting fibroblasts can potenlially receive RA signal from WAE cells. To identify genes that can be induced by retinoic acid in mouse fibroblast, we performed bulk RNA-seq using NIH3T3 cells.

2023-10-26 | GSE235732 | GEO

Retinoic acid signaling during priming licenses intestinal CD103+ CD8 TRM cell differentiation

Project description:Retinoic acid signaling during priming licenses intestinal CD103+ CD8 TRM cell differentiation

| PRJNA929262 | ENA

Retinoic acid signaling during priming licenses intestinal CD103+ CD8 TRM cell differentiation

Project description:CD8 tissue-resident memory T (TRM) cells provide front-line protection at barrier tissues; however, mechanisms regulating TRM cell development are not completely understood. Priming dictates the migration of effector T cells to the tissue, while factors in the tissue induce in situ TRM cell differentiation. Whether priming also regulates in situ TRM cell differentiation uncoupled from migration is unclear. Here, we demonstrate that T cell priming in the mesenteric lymph nodes (MLN) regulates CD103+ TRM cell differentiation in the intestine. In contrast, T cells primed in the spleen were impaired in the ability to differentiate into CD103+ TRM cells after entry into the intestine. MLN priming initiated a CD103+ TRM cell gene signature and licensed rapid CD103+ TRM cell differentiation in response to factors in the intestine. Licensing was regulated by retinoic acid signaling and primarily driven by factors other than CCR9 expression and CCR9-mediated gut homing. Thus, the MLN is specialized to promote intestinal CD103+ CD8 TRM cell development by licensing in situ differentiation.

2023-02-13 | GSE223983 | GEO

ISX is a retinoic acid-sensitive gatekeeper that controls intestinal beta,beta-carotene absorption and vitamin A production.

Project description:The uptake of dietary lipids from the small intestine is a complex process that depends on the activities of specific membrane receptors with yet unknown regulatory mechanisms. Using both mouse models and human cell lines, we show here that intestinal lipid absorption by the scavenger receptor class B type 1 (SR-BI) is subject to control by retinoid signaling. Retinoic acid via retinoic acid receptors induced expression of the intestinal transcription factor ISX. ISX then repressed the expression of SR-B1 and the carotenoid-15,15'-oxygenase Bcmo1. BCMO1 acts downstream of SR-BI and converts absorbed beta,beta-carotene to the retinoic acid precursor, retinaldehyde. Using BCMO1-knockout mice, we demonstrated increased intestinal SR-BI expression and systemic beta,beta-carotene accumulation. SR-BI-dependent accumulation of beta,beta-carotene was prevented by dietary retinoids that induced ISX expression. Thus, our study revealed a diet-responsive regulatory network that controls beta,beta-carotene absorption and vitamin A production by negative feedback regulation. The role of SR-BI in the intestinal absorption of other dietary lipids, including cholesterol, fatty acids, and tocopherols, implicates retinoid signaling in the regulation of lipid absorption more generally and has clinical implications for diseases associated with dyslipidemia.

| S-EPMC2874479 | biostudies-other

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