Girish C, Sanjay S. Role of immune dysfunction in drug induced liver injury. World J Hepatol 2021; 13(11): 1677-1687 [PMID: 34904037 DOI: 10.4254/wjh.v13.i11.1677]
Corresponding Author of This Article
Chandrashekaran Girish, MSc, PhD, Additional Professor, Department of Pharmacology, Jawaharlal Institute of Postgraduate Medical Education and Research, Puducherry 605006, India. gcnx@rediffmail.com
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Minireviews
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. Nov 27, 2021; 13(11): 1677-1687 Published online Nov 27, 2021. doi: 10.4254/wjh.v13.i11.1677
Role of immune dysfunction in drug induced liver injury
Chandrashekaran Girish, Sukumaran Sanjay
Chandrashekaran Girish, Sukumaran Sanjay, Department of Pharmacology, Jawaharlal Institute of Postgraduate Medical Education and Research, Puducherry 605006, India
Author contributions: Girish C and Sanjay S contributed equally to this work; Girish C planned the contents and edited the manuscript; Sanjay S reviewed the literature, wrote the manuscript; All authors have read and approved the final manuscript.
Conflict-of-interest statement: The authors have no conflicts of interest to disclose.
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: http://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Chandrashekaran Girish, MSc, PhD, Additional Professor, Department of Pharmacology, Jawaharlal Institute of Postgraduate Medical Education and Research, Puducherry 605006, India. gcnx@rediffmail.com
Received: April 3, 2021 Peer-review started: April 3, 2021 First decision: July 6, 2021 Revised: July 15, 2021 Accepted: September 16, 2021 Article in press: September 16, 2021 Published online: November 27, 2021
Abstract
Drug-induced liver injury (DILI) is one of the leading causes of liver failure and withdrawal of drugs from the market. A poor understanding of the precipitating event aetiology and mechanisms of disease progression has rendered the prediction and subsequent treatment intractable. Recent literature suggests that some drugs can alter the liver’s repair systems resulting in injury. The pathophysiology of DILI is complex, and immune dysfunction plays an important role in determining the course and severity of the disease. Immune dysfunction is influenced by the host response to drug toxicity. A deeper understanding of these processes may be beneficial in the management of DILI and aid in drug development. This review provides a structured framework presenting DILI in three progressive stages that summarize the interplay between drugs and the host defence networks.
Core Tip: This review demonstrates the critical role of the immune system in the progression of drug-induced liver injury and also in determining the severity of the damage. Drugs affect the normal functioning of hepatocytes through several direct and indirect mechanisms leading to the dysfunctional immune response. The major effector cells in amplifying liver damage are Kupffer cells, monocytes and neutrophils. Genetic predispositions and environmental factors also make individuals vulnerable to immune dysfunction.
