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Analysis of immunoglobulin G subclass in the serum antibody responses of alveolar echinococcosis patients after surgical treatment and chemotherapy as an aid to assessing the outcome

子类 医学 化疗 抗体 免疫学 免疫球蛋白G 内科学
作者
Hao Wen,Solange Bresson‐Hadni,Dominique A. Vuitton,D Lenys,Bingbing Yang,Z.X. Ding,Philip S. Craig
出处
期刊:Transactions of The Royal Society of Tropical Medicine and Hygiene [Oxford University Press]
卷期号:89 (6): 692-697 被引量:25
标识
DOI:10.1016/0035-9203(95)90449-2
摘要

Immunoglobulin G (IgG) subclass-specific antibody responses were evaluated for the follow-up of alveolar echinococcosis (AE) patients. Seventy-four sequentially collected sera from 25 Chinese and French AE cases who underwent surgery including hepatectomy, liver transplant and/or chemotherapy were analysed quantitatively and qualitatively during the clinical follow-up period. These AE patients were classified in 4 groups--cured, improved, stabilized, or aggravated. Serum antibody levels of the subclasses IgG1 and IgG4 were significantly higher in the AE patients than in healthy controls. IgG1 and IgG4 isotypes in AE patients were the most sensitive IgG antibody response in an enzyme-linked immunosorbent assay (ELISA) and in binding to antigens of 44kDa, 35kDa, 21kDa and 17.5kDa in an Echinococcus multilocularis protoscolex extract after Western blotting. In AE cases classed as cured or improved, IgG subclass antibody levels tended to decrease earlier than total IgG levels, especially IgG4 antibody levels which became negative within one year after successful treatment. IgG4 antibody levels also decreased in most of the improved cases. Increasing or unchanged levels of IgG4 and IgG1 antibodies were demonstrated in both stabilized and aggravated AE cases using both ELISA and immunoblot assays. Reappearance of specific IgG4 antibodies was a strong indication of recurrence, especially in liver transplant patients. Combined quantitative and qualitative assessment of IgG1 and IgG4 antibodies may be potentially useful for the serological follow-up of human AE.
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