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Mechanistic target of rapamycin complex 1 orchestrates the interplay between hepatocytes and Kupffer cells to determine the outcome of immune-mediated hepatitis

ABSTRACT: Mechanistic target of rapamycin complex 1 orchestrates the interplay between hepatocytes and Kupffer cells to determine the outcome of immune-mediated hepatitis

PROVIDER: PRJNA904947 | ENA |

REPOSITORIES: ENA

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Mechanistic target of rapamycin complex 1 orchestrates the interplay between hepatocytes and Kupffer cells to determine the outcome of immune-mediated hepatitis

Project description:The cell-cell interaction between hepatocytes and Kupffer cells (KCs) is crucial for maintaining liver homeostasis, and the loss of KCs and hepatocytes is known to represent a common pathogenic phenomenon in autoimmune hepatitis. Until now, the mechanisms of cell-cell interaction between hepatocytes and KCs involved in immune-mediated hepatitis remains unclear. Here we dissected the impact of activated mTORC1 on the cell-cell interaction of KCs and hepatocyte in immune-mediated hepatitis. In the liver from patients with AIH and mice administrated with Con-A, mTORC1 was activated in both KCs and hepatocytes. The activated mTORC1 signal in hepatocytes with Con-A challenge caused a markedly production of miR-329-3p. Upregulated miR-329-3p inhibited SGMS1 expression in KCs through paracrine, resulting in the death of KCs. Most of maintained KCs were p-S6 positive and distributed in hepatocyte mTORC1 negative area. The activation of mTORC1 enabled KCs expressed complement factor B (CFB) to enhance the complement alternative system, which produced more complement factors to aggravate liver injury. Our findings remonstrate a heterogeneous role of mTORC1 in specific cell type for maintaining tolerogenic liver environment, and will form the basis for the development of new interventions against immune-mediated hepatitis.

2022-12-07 | GSE218700 | GEO

Mechanistic target of rapamycin complex 1 orchestrates the interplay between hepatocytes and Kupffer cells to determine the outcome of immune-mediated hepatitis.

| S-EPMC9734196 | biostudies-literature

Changes in RNA levels following inhibition of mechanistic target of rapamycin

Project description:This study aimed to identify changes in RNA levels after inhibiting the mechanistic target of rapamycin using RNA sequencing.

2025-09-20 | GSE304701 | GEO

Assessing protein level changes following inhibition of the mechanistic target of rapamycin

Project description:This study focused on determining changes in protein levels following inhibition of the mechanistic target of rapamycin using mass spectrometry analysis.

2025-09-20 | PXD049052 | Pride

Changes in RNA levels following inhibition of mechanistic target of rapamycin

Project description:Changes in RNA levels following inhibition of mechanistic target of rapamycin

| PRJNA1302361 | ENA

Determination of protein level changes following inhibition of the mechanistic target of rapamycin

Project description:This study aimed to identify changes in protein level after inhibiting the mechanistic target of rapamycin using mass spectrometry analysis

2023-07-27 | PXD041933 | Pride

Mechanistic Target of Rapamycin Complex 2 (mTORC2) regulation of the primary human trophoblast cell transcriptome

Project description:Mechanistic Target of Rapamycin Complex 2 (mTORC2) regulation of the primary human trophoblast cell transcriptome

| PRJNA771456 | ENA

Effects of rapamycin, torin1, and rapalink1 on RNA levels

Project description:This study aimed to identify changes in RNA levels after inhibiting the mechanistic target of rapamycin using RNA sequencing.

2023-07-27 | GSE229623 | GEO

RNAseq of Kupffer cells treated with IL2 and purifed Kupffer cells sub-populations (Kupffer Cell 1 and Kupffer Cell 2)

Project description:RNAseq of Kupffer cells treated with IL2 and purifed Kupffer cells sub-populations (Kupffer Cell 1 and Kupffer Cell 2)

| PRJNA638642 | ENA

Rapamycin-Gliadin Composite Nanoparticles Enhance Hepato-Splenic Dialogue for Gluten Tolerance in Celiac Disease

Project description:Background Celiac disease (CeD) is an autoimmune disorder triggered by gluten, with gliadin as the primary antigen. Therapies targeting gliadin to induce antigen-specific immune tolerance are of significant interest. This study investigates the therapeutic potential of a novel rapamycin-gliadin composite nanoparticle (PLN-GR) in enhancing Kupffer cell-mediated hepato-splenic dialogue to promote gluten tolerance in CeD. Methods Rapamycin-gliadin composite nanoparticles were synthesized using a precipitation self-assembly method and characterized for size, zeta potential, and cellular uptake. A CeD delayed-type hypersensitivity (DTH) mouse model was employed to evaluate the immunomodulatory effects of PLN-GR. Cellular biodistribution, immune phenotyping, and metabolic assessments were conducted to elucidate the nanoparticles' mechanism of action. Results Rapamycin-gliadin composite nanoparticles effectively targeted the liver and were internalized by Kupffer cells, inducing a tolerogenic phenotype. In vivo treatment with PLN-GR ameliorated systemic and intestinal inflammation in the CeD DTH mouse model, evidenced by reduced paw swelling and intestinal histopathology. The nanoparticles induced a metabolic shift from glycolysis to oxidative phosphorylation in macrophages, associated with increased itaconate production. This metabolic reprogramming was linked to an increase in PD-L1+ tolerogenic dendritic cells and a decrease in Th1 cell counts in the spleen. Conclusion The study demonstrates that rapamycin-gliadin nanoparticles can induce antigen-specific tolerance in CeD by modulating hepatic and splenic immune responses. The findings suggest a potential therapeutic strategy for CeD by enhancing immunometabolic reprogramming and inter-organ communication.

2025-07-30 | GSE275197 | GEO

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