Division of Rheumatology, Allergy and Clinical Immunology, University of California at Davis School of Medicine, Davis, CA 95616, USA.
Trends Mol Med. 2012 Oct;18(10):577-82. doi: 10.1016/j.molmed.2012.07.005. Epub 2012 Aug 21.
The serologic hallmark of primary biliary cirrhosis (PBC) is the presence of antimitochondrial autoantibodies (AMAs) directed against the E2 subunit of the pyruvate dehydrogenase complex (PDC-E2). The PBC-related autoepitope of PDC-E2 contains lipoic acid, and previous work has demonstrated that mimics of lipoic acid following immunization of mice lead to a PBC-like disease. Furthermore, approximately one-third of patients who have ingested excessive amounts of acetaminophen (paracetamol) develop AMA of the same specificity as patients with PBC. Quantitative structure-activity relationship (QSAR) data indicates that acetaminophen metabolites are particularly immunoreactive with AMA, and we submit that in genetically susceptible hosts, electrophilic modification of lipoic acid in PDC-E2 by acetaminophen or similar drugs can facilitate a loss of tolerance and lead to the development of PBC.
原发性胆汁性肝硬化(PBC)的血清学标志是存在针对丙酮酸脱氢酶复合物(PDC-E2)E2 亚单位的抗线粒体自身抗体(AMAs)。PDC-E2 的 PBC 相关自身抗原含有硫辛酸,以前的工作表明,在给小鼠免疫模拟硫辛酸后,会导致类似于 PBC 的疾病。此外,大约三分之一摄入过量对乙酰氨基酚(扑热息痛)的患者会产生与 PBC 患者相同特异性的 AMA。定量构效关系(QSAR)数据表明,对乙酰氨基酚代谢物与 AMA 的免疫反应特别强,我们认为,在遗传易感宿主中,对乙酰氨基酚或类似药物对 PDC-E2 中硫辛酸的亲电修饰可以促进耐受性丧失,并导致 PBC 的发展。