Treichel U, Gerken G, Rossol S, Rotthauwe H W, Meyer zum Büschenfelde K H, Poralla T
1st Department of Internal Medicine, University of Mainz, Germany.
J Hepatol. 1993 Aug;19(1):55-63. doi: 10.1016/s0168-8278(05)80176-x.
The hepatic asialoglycoprotein receptor (ASGPR) was recently identified as a target antigen for both humoral and cellular immune response in inflammatory liver diseases. Thereby anti-ASGPR autoantibodies directed against human substrate were closely associated with autoimmune chronic active hepatitis. The present study compares the occurrence, titer and immunoglobulin classification of anti-human(h-)-ASGPR antibodies in 23 patients with newly diagnosed autoimmune chronic hepatitis before and after initiation of immunosuppressive therapy to 22 patients with autoimmune hepatitis in remission. Additionally, 1-year follow-up examinations of 42 patients with HBsAg-positive chronic hepatitis and of 32 patients with chronic hepatitis C receiving recombinant interferon-alpha were included. Nineteen of 23 patients with newly diagnosed and 9/22 with autoimmune hepatitis in remission, 5/42 with untreated chronic hepatitis B and 5/32 patients with chronic hepatitis C exhibited anti-h-ASGPR at the beginning of the study. In autoimmune hepatitis anti-h-ASGPR were found in higher titers (median > 1:1000) than in viral hepatitis (maximum 1:400). After initiation of immunosuppressive therapy in autoimmune hepatitis anti-h-ASGPR decreased sharply. Eight of 19 patients eliminated anti-h-ASGPR within 18 months in contrast to 11 patients with persistent anti-h-ASGPR titer over 18 months and longer. Anti-h-ASGPR with maximum titer of 1:600 were detected in 5 patients with chronic hepatitis B (transiently in 4/5 patients) and in 2 patients with chronic hepatitis C during interferon-alpha. Anti-h-ASGPR were from immunoglobulin classes IgG and IgM in cases with untreated autoimmune hepatitis and chronic hepatitis B and C exhibiting mainly IgG2-subclass in autoimmune and IgG4 in viral hepatitis.(ABSTRACT TRUNCATED AT 250 WORDS)
肝去唾液酸糖蛋白受体（ASGPR）最近被确定为炎症性肝病中体液免疫和细胞免疫反应的靶抗原。因此，针对人类底物的抗ASGPR自身抗体与自身免疫性慢性活动性肝炎密切相关。本研究比较了23例新诊断的自身免疫性慢性肝炎患者在免疫抑制治疗开始前后抗人（h-）ASGPR抗体的发生率、滴度和免疫球蛋白分类，与22例处于缓解期的自身免疫性肝炎患者进行对比。此外，纳入了42例HBsAg阳性慢性肝炎患者和32例接受重组干扰素-α治疗的丙型肝炎患者的1年随访检查。在研究开始时，23例新诊断患者中有19例、22例缓解期自身免疫性肝炎患者中有9例、42例未治疗的慢性乙型肝炎患者中有5例以及32例丙型肝炎患者中有5例表现出抗h-ASGPR。在自身免疫性肝炎中发现抗h-ASGPR的滴度（中位数>1:1000）高于病毒性肝炎（最高1:400）。自身免疫性肝炎患者开始免疫抑制治疗后，抗h-ASGPR急剧下降。19例患者中有8例在18个月内消除了抗h-ASGPR，而11例患者的抗h-ASGPR滴度在18个月及更长时间内持续存在。在5例慢性乙型肝炎患者（4/5例为短暂性）和2例丙型肝炎患者接受干扰素-α治疗期间检测到最高滴度为1:600的抗h-ASGPR。未治疗的自身免疫性肝炎、慢性乙型肝炎和丙型肝炎患者的抗h-ASGPR来自免疫球蛋白类别IgG和IgM，在自身免疫性疾病中主要为IgG2亚类，在病毒性肝炎中为IgG4。（摘要截取自250字）
