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Cells
Special Issues
Pathophysiological Mechanisms of Cholestatic and Metabolic-Associated Fatty Liver Disease
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Pathophysiological Mechanisms of Cholestatic and Metabolic-Associated Fatty Liver Disease

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: closed (31 May 2024) | Viewed by 1370

Special Issue Editor

Prof. Dr. Jan G. Hengstler

E-Mail Website
Guest Editor
Head of Research Group, Systemtoxicology–Leibniz Research Centre for Working Environment and Human Factors (IfADo), Dortmund, Germany
Interests: liver physiology; liver pathology; liver imaging
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Metabolic-associated fatty liver disease (MAFLD) and cholestatic liver diseases represent a major health problem. Interestingly, both disease groups share some key mechanisms that can be therapeutically addressed, including specific nuclear receptors controlling glucose, lipid and bile acid homeostasis, immune cell infiltration, fibrosis, proliferation and the compromise of transport processes. The Special Issue will focus on pathomechanisms and/or therapeutic interventions in cell systems, animal models or in patients. In this Special Issue, an overview about the currently available knowledge and recent findings regarding the development, progression, molecular pathways, and mechanisms of these diseases is given.

Prof. Dr. Jan G. Hengstler
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • steatosis
  • steatohepatitis
  • bile flux
  • inflammation
  • FXR

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Published Papers (1 paper)

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Research

20 pages, 9139 KB  
Article
Western Diet Dampens T Regulatory Cell Function to Fuel Hepatic Inflammation in Metabolic Dysfunction-Associated Steatotic Liver Disease
by Sudrishti Chaudhary, Ravi Rai, Pabitra B. Pal, Dana Tedesco, Daniel Rossmiller, Biki Gupta, Aatur D. Singhi, Satdarshan P. Monga, Arash Grakoui, Smita S. Iyer and Reben Raeman
Cells 2026, 15(2), 165; https://doi.org/10.3390/cells15020165 - 16 Jan 2026
Cited by 1 | Viewed by 842
Abstract
The immunosuppressive T regulatory cells (Tregs) regulate immune responses and maintain immune homeostasis, yet their functions in metabolic dysfunction-associated steatotic liver disease (MASLD) remain controversial. Here we report increased accumulation of Tregs and effector T cells within the liver parenchyma of mice fed [...] Read more.
The immunosuppressive T regulatory cells (Tregs) regulate immune responses and maintain immune homeostasis, yet their functions in metabolic dysfunction-associated steatotic liver disease (MASLD) remain controversial. Here we report increased accumulation of Tregs and effector T cells within the liver parenchyma of mice fed a Western diet (WD). This pattern was also observed in MASH patients, where an increase in intrahepatic Tregs was noted. In the absence of adaptive immune cells in Rag1 KO mice, WD promoted accumulation of intrahepatic neutrophils and macrophages and exacerbated hepatic inflammation and fibrosis. Similarly, targeted Treg depletion exacerbated WD-induced hepatic inflammation and fibrosis. In Treg-depleted mice, hepatic injury was associated with increased accumulation of neutrophils, macrophages, and activated T cells in the liver. Conversely, induction of Treg numbers using recombinant IL2/αIL2 mAb cocktail reduced hepatic steatosis, inflammation, and fibrosis in WD-fed mice. Analysis of intrahepatic Tregs from WD-fed mice revealed a phenotypic signature of impaired Treg function in MASLD. Ex vivo functional studies showed that glucose and palmitate, but not fructose, impaired the immunosuppressive ability of Treg cells. The findings indicate that the liver microenvironment in MASLD impairs the ability of Tregs to suppress effector immune cell activation, thus perpetuating chronic inflammation and driving MASLD progression. Full article
(This article belongs to the Special Issue Pathophysiological Mechanisms of Cholestatic and Metabolic-Associated Fatty Liver Disease)
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