Palmer J M, Kirby J A, Jones D E J
Centre for Liver Research, University of Newcastle, Newcastle-upon-Tyne, UK.
Clin Exp Immunol. 2002 Aug;129(2):191-7. doi: 10.1046/j.1365-2249.2002.01948.x.
The chronic liver disease primary biliary cirrhosis (PBC) is characterised by autoreactive B-cell and T-cell responses directed against mitochondrial antigens. In recent years these responses have been extensively characterised and the principal PBC associated autoantigen identified as pyruvate dehydrogenase complex (PDC). The identification of anti-PDC responses (present in over 95% of PDC patients) has given rise to important questions pertinent to our understanding of the pathogenesis of PBC. What specific role to anti-PDC responses play in target cell damage? How and why does immune tolerance break down to as highly conserved and ubiquitously expressed self-antigen as PDC? Why does breakdown in tolerance to an antigen present in all nucleated cells result in damage restricted to the intra-hepatic bile ducts? In attempting to answer these key questions we have, in this review, proposed a unifying hypothesis for the pathogenesis of PBC.
慢性肝病原发性胆汁性肝硬化(PBC)的特征是针对线粒体抗原的自身反应性B细胞和T细胞反应。近年来,这些反应已得到广泛表征,并且主要的PBC相关自身抗原被鉴定为丙酮酸脱氢酶复合物(PDC)。抗PDC反应的鉴定(存在于超过95%的PBC患者中)引发了与我们对PBC发病机制的理解相关的重要问题。抗PDC反应在靶细胞损伤中起什么具体作用?免疫耐受是如何以及为何会对像PDC这样高度保守且普遍表达的自身抗原发生破坏的?为什么对所有有核细胞中都存在的一种抗原的耐受破坏会导致损伤仅限于肝内胆管?在试图回答这些关键问题时,我们在本综述中提出了一个关于PBC发病机制的统一假说。