抗线粒体抗体阳性与抗线粒体抗体阴性的原发性胆汁性肝硬化的
门脉细胞浸润的比较分析
大量证据表明PBC患者存在异常B细胞免疫应答，包括抗线粒体抗体（AMAs）的出现，然而，最近由PBC鼠模型得出的研究提示B细胞可能也有调节功能，而且，这些模型中B细胞的缺失也确实造成疾病加重。绝大多数的PBC患者都易检测到抗线粒体抗体，但有小部分，即使应用重组诊断技术，亦检测不到AMA，这个问题促使我们去检测在AMA阳性患者与AMA阴性患者门脉区周围所浸润的B细胞的种类，因为他们具有不易察觉的临床作用。 一个重要的结果就是AMA阳性的PBC门脉区胆管破坏程度明显轻于其阴性者。AMA阴性患者的胆管区CD 5+ 细胞浸润明显增加，而且B细胞浸润水平于胆管破坏早期更严重。CD5+和CD20+细胞在胆管侵入区的浸润强度与早期胆管上皮破坏有关，但其在胆管消失期减少，除了CD5+细胞，其持续存在并多于CD20+细胞。 结论：我们的数据提示B细胞自身免疫对PBC所特有门脉破坏可能起到调节作用。门脉细胞浸润的比较分析
吉林大学第一医院肝胆胰内科 李银萍 摘译
本文首次发表于[Hepatology, 2012, 55(5):1495-1506]
Comparative Analysis of Portal Cell Infiltrates in Antimitochondrial Autoantibody–Positive Versus Antimitochondrial Autoantibody Negative Primary Biliary Cirrhosis
Substantial evidence supports dysregulated B-cell immune responses in patients with primary biliary cirrhosis (PBC), including the presence of serum antimitochondrial antibodies (AMAs). However, recent reports from murine models of PBC suggest that B cells may also provide regulatory function, and indeed the absence of B cells in such models leads to exacerbation of disease.The vast majority of patients with PBC have readily detectable AMAs, but a minority (<5%) are AMA negative (AMA2), even with recombinant diagnostic technology. This issue prompted us to examine the nature of B-cell infiltrates surrounding the portal areas in AMA-positive (AMA1) and AMA2 patients, because they display indistinguishable clinical features.Of importance was the finding that the degree of bile duct damage around the portal areas was significantly milder in AMA1 PBC than those observed in AMA2 PBC patients. The portal areas from AMA2 patients had a significant increase of cluster of differentiation (CD)5+ cells infiltrating the ductal regions,and the levels of B-cell infiltrates were worse in the early phase of bile duct damage.The magnitude of CD5+ and CD20+ cellular infiltrates within areas of ductal invasion is associated with the first evidence of damage of biliary duct epithelia, but becomes reduced in the ductopenia stage, with the exception of CD5+ cells, which remain sustained and predominate over CD20+ cells. Conclusion: Our data suggest a putative role of B-cell autoimmunity in regulating the portal destruction characteristic of PBC.
