Bhatnagar P, Eid N. Rapamycin nanoparticles suppress autoreactive lymphocytes and reduce anti-mitochondrial antibodies in primary biliary cholangitis: Mechanisms and implications. World J Hepatol 2025; 17(9): 110674 [DOI: 10.4254/wjh.v17.i9.110674]
Corresponding Author of This Article
Nabil Eid, MD, PhD, Associate Professor, Department of Human Biology, Division of Anatomy, School of Medicine, IMU University, Kuala Lumpur 57000, Malaysia. nabilsaleheid@imu.edu.my
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Editorial
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Hepatol. Sep 27, 2025; 17(9): 110674 Published online Sep 27, 2025. doi: 10.4254/wjh.v17.i9.110674
Rapamycin nanoparticles suppress autoreactive lymphocytes and reduce anti-mitochondrial antibodies in primary biliary cholangitis: Mechanisms and implications
Payal Bhatnagar, Nabil Eid
Payal Bhatnagar, Department of Pharmaceutical Technology, School of Pharmacy, IMU University, Kuala Lumpur 57000, Malaysia
Nabil Eid, Department of Human Biology, Division of Anatomy, School of Medicine, IMU University, Kuala Lumpur 57000, Malaysia
Author contributions: Bhatnagar P wrote the manuscript; Eid N designed the figure, wrote and approved the final draft of the manuscript. All authors have read and approved the final manuscript.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Open Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Nabil Eid, MD, PhD, Associate Professor, Department of Human Biology, Division of Anatomy, School of Medicine, IMU University, Kuala Lumpur 57000, Malaysia. nabilsaleheid@imu.edu.my
Received: June 12, 2025 Revised: June 24, 2025 Accepted: August 11, 2025 Published online: September 27, 2025 Processing time: 105 Days and 18.7 Hours
Abstract
Primary biliary cholangitis (PBC) is an autoimmune disease characterized by the selective destruction of intrahepatic small bile ducts, primarily by infiltrating lymphocytes, and has limited therapeutic options. A growing body of evidence suggests that nanoparticles encapsulating rapamycin (ImmTOR) can suppress autoreactive lymphocytes and reduce inflammatory cytokine levels in various autoimmune diseases. In a recent study, Yang et al investigated the therapeutic effects of ImmTOR in a mouse model of PBC. ImmTOR treatment reduced the expression and number of CD4+ T cells, CD8+ T cells, and B cells isolated from the liver and spleen, improved liver inflammation and enzyme levels, and was associated with a concomitant decrease in anti-mitochondrial antibody levels. In this editorial, we highlight the significance of these findings, focusing on the potential mechanisms by which ImmTOR suppresses hepatic autoreactive T cells and reduces anti-mitochondrial antibody levels, ultimately improving liver pathology, through pathways such as mammalian target of rapamycin inhibition and autophagy restoration. We also offer a perspective on future research directions for PBC in both animal models and in vitro studies.
Core Tip: Primary biliary cholangitis (PBC) is an autoimmune disease with limited therapeutic options. A recent study using a mouse model of PBC found that nanoparticles encapsulating rapamycin treatment reduced the levels of autoreactive T cells and B cells in the liver and spleen, improved liver inflammation and enzyme levels, and was associated with a concomitant decrease in anti-mitochondrial antibody levels. These findings indicate that nanoparticles encapsulating rapamycin may improve liver pathology in the PBC mouse model through mammalian target of rapamycin inhibition and potential autophagy restoration, suggesting it could represent a novel therapeutic option for this chronic disease.
