Special Issue "Molecular Mechanisms of Drug-Induced Liver Injury: Emerging Role of Innate and Adaptive Immunity"

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Medical Biology".

Deadline for manuscript submissions: 31 August 2022 | Viewed by 183

Special Issue Editors

Dr. Bibo Ke
E-Mail Website
Guest Editor
The Dumont-UCLA Transplant Center, Department of Surgery, David Geffen School of Medicine at UCLA, The University of California at Los Angeles, 10833 Le Conte Ave, Los Angeles, CA 90095, USA
Interests: macrophage; innate immunity; inflammation; cell death; liver injury
Dr. Changyong Li
E-Mail Website
Guest Editor
Department of Physiology, School of Basic Medical Sciences, Wuhan University, Wuhan 430071, China
Interests: immune regulation; liver inflammation; hepatic fibrosis

Special Issue Information

Dear Colleagues,

Drug-induced liver injury (DILI) is a major cause of acute liver failure (ALF), with associated mortality and the need for liver transplantation. A variety of drugs can cause DILI, including antipyretic analgesics, chemotherapy, and immunosuppressive agents; hypoglycemic and lipid-lowering drugs; anti-bacterial, anti-fungal, and anti-viral drugs; anti-depressant agents; and herbal medicine. Accumulating evidence indicates that the mechanisms of DILI might also be involved in oxidative and endoplasmic reticulum (ER) stress through reactive oxygen species (ROS), which impair mitochondrial functions, leading to apoptosis or necrosis-mediated cell death. Recent studies suggest that the pathogenesis of DILI is associated with innate and adaptive immune responses. The liver is an immunological organ that contains many immune cells, including innate immune cells (Kupffer cells, neutrophils, dendritic cells, NK cells, etc.) and intrahepatic lymphocytes. The activation of innate immune cells, such as Kupffer cells, induces innate immune responses by recognizing the endogenous molecules called damage-associated molecular patterns (DAMPs) released from drug-damaged hepatocytes, resulting in sterile inflammation. Moreover, drugs and their metabolites can be recognized by the T cell receptors (TCRs) and induce drug-specific T cell responses. Although studies suggest that innate and adaptive responses play a role in the mechanism of DILI, the early molecular events and innate and adaptive immune signaling cascades that trigger drug-induced hepatotoxicity are still poorly defined. We invite investigators to submit original research or review articles to document new data, describe state-of-the-art experimental models, or formulate new ideas to promote these advancements. We are interested in articles describing basic research in in vivo and in vitro models. Potential topics include, but are not limited to:

  • Mechanisms of Kupffer cells, neutrophils, dendritic cells, NK cells, and T cells in the pathogenesis of drug-induced liver injury;
  • Pathogen recognition and immune/inflammatory signaling in drug-induced liver injury;
  • Identification of new molecular biomarkers in drug-induced liver injury;
  • Roles of endogenous molecules in the pathogenesis of drug-induced liver injury;
  • New insights in molecular signaling networks that regulate innate adaptive immunity in drug-induced liver injury;
  • Genome-wide association studies in drug-induced liver injury.

Dr. Bibo Ke
Dr. Changyong Li
Guest Editors

Manuscript Submission Information

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2000 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.


  • innate immunity
  • adaptive immunity
  • inflammation
  • ER stress
  • cell death
  • apoptosis
  • necroptosis
  • autophagy
  • pyroptosis
  • ferroptosis
  • liver injury

Published Papers

This special issue is now open for submission.
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