Detection of an IgM antiidiotype directed against anti-HBs in hepatitis B patients
Article first published online: 5 DEC 2005
Copyright © 1985 American Association for the Study of Liver Diseases
Volume 5, Issue 5, pages 758–762, September/October 1985
How to Cite
Troisi, C. L. and Hollinger, F. B. (1985), Detection of an IgM antiidiotype directed against anti-HBs in hepatitis B patients. Hepatology, 5: 758–762. doi: 10.1002/hep.1840050509
- Issue published online: 5 DEC 2005
- Article first published online: 5 DEC 2005
- Manuscript Accepted: 1 JUL 1985
- Manuscript Received: 11 MAR 1985
- National Institute of Allergy and Infectious Diseases. Grant Numbers: AI 18674–01, N01-AI-92609
- National Institutes of Health
- Gulf Coast Regional Blood Center. Grant Number: DAMD 17–82C–2155
- United States Army Medical Research and Development Command
An IgM-specific anti-[anti-HBs] antibody was detected by radioimmunoassay using anti-IgM-coated beads and 125I-labeled anti-HBs. This antiidiotype was found only in the sera of hepatitis B virus-infected patients, both acute and chronic. However, not all HBsAg-positive patients exhibited this reaction, and activity was correlated with the presence of HBeAg. Approximately 93% of sera that contained antiidiotype activity also contained HBeAg. Conversely, 70% of the sera positive for HBeAg reacted in the IgM assay. No correlation was observed between the presence of antiidiotype and rheumatoid factor or elevated SGPT levels.
Two approaches were used to determine whether the reactive moiety was an IgM anti-[anti-HBs] as postulated or an IgM anti-HBs/HBsAg complex. It was shown that chicken anti-HBs sera, which does not share the common idiotype of human and other mammalian anti-HBs, did not block a positive reaction in this radioimmunoassay even though it specifically bound HBsAg. It was also demonstrated that treatment with polyethylene gylcol, which will precipitate IgM anti-HBs/HBsAg activity, did not precipitate the reactive moiety in 6 of 7 sera tested, lending further evidence to the existence of an IgM antiidiotype in these patients.
It is suggested that this antiidiotype directed against anti-HBs may be involved in a defective feedback mechanism resulting in the suppression of production of anti-HBs and maintenance of the carrier state.