Special Issue "Molecular Mechanisms of Drug-Induced Liver Injury: Emerging Role of Innate and Adaptive Immunity"
Deadline for manuscript submissions: 31 August 2022 | Viewed by 183
Interests: macrophage; innate immunity; inflammation; cell death; liver injury
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
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- innate immunity
- adaptive immunity
- ER stress
- cell death
- liver injury