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Mechanisms of immune checkpoint inhibitormediated liver injury

Acta Pharmaceutica Sinica B 2021年第12期11卷 3727-3739页

作者： layla shojaie Myra Ali Andrea Iorga Lily Dara Division of Gastrointestinal and Liver Diseases Department of MedicineKeck School of MedicineUniversity of Southern CaliforniaLos AngelesCA 90033USA Research Center for Liver Disease Keck School of MedicineUniversity of Southern CaliforniaLos AngelesCA 90033USA Keck School of Medicine University of Southern CaliforniaLos AngelesCA 90033USA U.S.Food and Drug Administration Center for Devices and Radiological HealthSilver SpringMD 20993USA UMBC Center for Accelerated Real Time Analytics University of MarylandBaltimore CountyBaltimoreMD 21250USA

The immune checkpoints,cytotoxic T-lymphocyte-associated antigen 4(CTLA-4) and programmed cell death protein-1/ligand-1(PD-1/PD-L1) are vital contributors to immune resulation and *** immune checkpoint inhibitors(ICIs) have revolutionized cancer therapy;however,they come with the cost of immune related adverse events involving multiple organs such as the *** to its constant expo sure to foreign antigens,the liver has evolved a high capacity for immune tolerance,therefore,blockade of the immune checkpoints can result in aberrant immune activation affecting the liver in up to 20% of patients depending on the agent(s) used and underlying *** type of hepatotoxicity is termed immune mediated liver injury from checkpoint inhibitors(ILICI) and is more common when CTLA4 and PD-1/PDL1 are used in *** underlying mechanisms of this unique type of hepatotoxicity are not fully understood;however,the contribution of CD8^(+) cytotoxic T lymphocytes,various CD4^(+) T cells populations,cytokines,and the secondary activation of the innate immune system leading to liver injury have all been *** review summarizes our current understanding of the underlying mechanisms of liver injury in immunotherapy using animal models of ILICI and available patient data from clinical studies.

关键词： Hepatotoxicity DILI Immunotherapy Cell death Hepatocyte CTLA-4 PD-1 PD-L1 Necrosis Apoptosis

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