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| 1 | Immune mechanisms of idiosyncratic drug-induced liver injury显示文摘Idiosyncratic drug reactions(IDRs)continue to be an important issue.Specifically,idiosyncratic drug-induced liver injury(IDILI)is the most likely IDR to lead to drug withdrawal,and it accounts for a significant portion of all cases of acute liver failure.In addition,IDRs are unpredictable and their mechanisms are not well understood.There is increasing clinical evidence that most IDILI is immune mediated.Several immune mediated mechanistic hypotheses exist such as the hapten and danger hypothesis;however,they do not completely explain the idiosyncratic nature of these reactions.Extensive mechanistic studies are needed to better understand these reactions;however,it is impossible to do controlled experiments in humans,and previous animal models did not properly model IDILI.If IDILI is immune mediated and the major factor preventing liver injury in patients is immune tolerance,then a plausible method to develop an animal model of IDILI would be to impair immune tolerance.This hypothesis has shown promise in developing valid animal models of IDILI as demonstrated by a halothane induced liver injury mouse model developed by depleting myeloid derived suppressor cells(MDSCs),as well as an amodiaquine-,isoniazid-and nevirapine-induced liver injury mouse model developed by impairing immune tolerance by blocking PD-1 and CTLA-4,two immune checkpoint inhibitors.Further characterization and validation of these models is required;however,it is likely that they will make it possible to perform mechanistic studies that have been impossible in the past.Relevance for patients:Idiosyncratic drug-induced liver injury can be serious leading to liver transplantation or death.Their idiosyncratic nature makes mechanistic studies very difficult.However,with the development of the first animal model that is similar to the liver injury that occurs in humans,it will be possible to study the mechanisms involved.With a better mechanistic understanding it should be possible to test drug candidates and produce safer drugs.In addition,it should be possible to design better treatments when drug-induced liver injury does occur. | Alastair Mak Jack Uetrecht | 2017 | Journal of Clinical & Translational Research2017，3，1： | 2 |
| 2 | Demonstration of the metabolic pathway responsible for nevirapine-induced skin rash显示文摘 | Chen J Mannargudi BM Xu L Uetrecht J | 2008 | Chem Res Toxicol2008，21，9： | 1 |
| 3 | D-penicillamine-induced autoimmunity in the brown Norway rat:role for both T and non-T splenocytes in adoptive transfer of tolerance显示文摘 | Séguin B Masson MJ Uetrecht J | 2004 | Chem Res Toxicol2004，17，10： | 1 |
| 4 | Tolerance induced by low dose D-penicillamine in the brown Norway rat model of drug-induced autoimmunity is immune-mediated显示文摘 | Masson MJ Uetrecht JP | 2004 | Chem Res Toxicol2004，17，1： | 1 |
| 5 | Mechanisms of immune-mediated liver injury显示文摘 | Adams DH Ju C Ramaiah SK Uetrecht J Jaeschke H | 2010 | Toxicol Sci2010，115，2： | 1 |
| 6 | Peroxidase-mediated bioactivation of hydroxylated metabolites of carbamazepine and phenytoin显示文摘 | Lu W Uetrecht JP | 2008 | Drug Metab Dispos2008，36，8： | 1 |
| 7 | Golgi polarity does not correlate with speed or persistence of freely migrating fibroblasts显示文摘 | Uetrecht AC Bear JE | 2009 | Eur J Cell Biol2009，88，： | 1 |
| 8 | New concepts in immunology relevant to idiosyncratic drug reactions: the 'danger hypothesis' and innate immune system显示文摘 | Uetrecht JP | 1999 | Chem Res Toxicol1999，12，5： | 1 |
| 9 | Immune-mediated adverse drug reactions显示文摘 | Uetrecht J | 2009 | Chem Res Toxicol2009，22，1： | 1 |
| 10 | The contribution of N-hydroxylation and acetylati on to dapsone pharmacokinetics in normal subjects 显示文摘 | May D G Porter J A Uetrecht J P | 1990 | Clin Pharmacol Ther1990，48，6： | 1 |
| 11 | New concepts in immunology relevant to idiosyncratic drug reactions:the'danger hypothesis'and innate immune system显示文摘 | Uetrecht JP | 1999 | J Chemical Res Toxicol1999，12，5： | 1 |
| 12 | Mechanism of drug-induced lupus显示文摘 | Uetrecht JP | 1988 | Chem Res Toxicol1988，1，3： | 1 |
| 13 | Current understanding of the mechanisms of idiosyncratic drug-induced agranulocytosis显示文摘 | Johnston A Uetrecht J | 2015 | Expert Opin Drug Metab Toxicol2015，11，2： | 1 |
| 14 | Role of drug metabolism for breaking tolerance and the localization of drug hypersensitivity显示文摘 | Uetrecht J | 2005 | Toxicology2005，209，： | 1 |
| 15 | Direct oxidation and covalent binding of isoniazid to rodent liver and human hepatic microsomes:humans are more like mice than rats显示文摘 | Metushi I G Nakagawa T and Uetrecht J | 2012 | Chemical Research in Toxicology2012，25，11： | 1 |
| 16 | Effect of clozapine and olanzapine on neutrophil kinetics: implications for drug-inducedagranulocytosis显示文摘 | Ng W Kennar R Uetrecht J | 2014 | Chem Res Toxicol2014，27，7： | 1 |
| 17 | Possible bioactivation pathways of lamotrigine 显示文摘 | Lu W Uetrecht JP | 2007 | Drug Metab Dispos2007，35，7： | 1 |
| 18 | Idiosyncratic drug reactions: the reactive metabolite syndromes显示文摘 | Knowles SR Uetrecht J Shear NH | 2000 | Lancet2000，356，9241： | 1 |
| 19 | Role of animal models in the study of drug-induced hypersensitivity reactions 显示文摘 | Uetrecht J | 2006 | AAPS J2006，7，4： | 1 |
| 20 | Idiosyncratic drug reactions: the reactive metabolite syndromes显示文摘 | Knowles SR Uetrecht J Shear NH | 2000 | Lancet2000，356，9241： | 1 |
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