Advertisement

Research Article Free access | 10.1172/JCI113231

Activation of terminal components of complement in patients with Guillain-Barré syndrome and other demyelinating neuropathies.

C L Koski, M E Sanders, P T Swoveland, T J Lawley, M L Shin, M M Frank, and K A Joiner

Department of Neurology, University of Maryland School of Medicine, Baltimore 21201.

Find articles by Koski, C. in: JCI | PubMed | Google Scholar

Department of Neurology, University of Maryland School of Medicine, Baltimore 21201.

Find articles by Sanders, M. in: JCI | PubMed | Google Scholar

Department of Neurology, University of Maryland School of Medicine, Baltimore 21201.

Find articles by Swoveland, P. in: JCI | PubMed | Google Scholar

Department of Neurology, University of Maryland School of Medicine, Baltimore 21201.

Find articles by Lawley, T. in: JCI | PubMed | Google Scholar

Department of Neurology, University of Maryland School of Medicine, Baltimore 21201.

Find articles by Shin, M. in: JCI | PubMed | Google Scholar

Department of Neurology, University of Maryland School of Medicine, Baltimore 21201.

Find articles by Frank, M. in: JCI | PubMed | Google Scholar

Department of Neurology, University of Maryland School of Medicine, Baltimore 21201.

Find articles by Joiner, K. in: JCI | PubMed | Google Scholar

Published November 1, 1987 - More info

Published in Volume 80, Issue 5 on November 1, 1987
J Clin Invest. 1987;80(5):1492–1497. https://doi.org/10.1172/JCI113231.
© 1987 The American Society for Clinical Investigation
Published November 1, 1987 - Version history
View PDF
Abstract

In the present study, the role of antiperipheral nerve myelin antibody (anti-PNM Ab) in demyelination by generating the terminal attack complex (C5b-9) of complement was explored in patients with Guillain-Barré syndrome (GBS) and other demyelinating neuropathies. The presence in serum of SC5b-9, an inactive C5b-9 containing S protein, was assessed quantitatively by enzyme-linked immunosorbent assay using an antibody (Ab) to neoantigens expressed on C9 when complexed with C5b-8 or after tubular polymerization. SC5b-9 was detected in all 19 GBS, four patients with paraprotein-associated neuropathy and five of six patients with chronic recurrent polyneuritis. No SC5b-9 was detected in 10 normal controls. Kinetic studies from six GBS patients showed the highest values of SC5b-9 on the 3rd to 5th d of admission; in contrast, the anti-PNM Ab were highest on the day of admission. Anti-PNM Ab fell rapidly to very low levels by the 15th to 20th d. SC5b-9 declined with similar kinetics to undetectable levels by the 30th d. Levels of Ab and SC5b-9 did not quantitatively correlate with soluble immune complexes in these patients' serum. Membrane-bound C5b-9 was also detected by immunohistochemistry in the peripheral nerves from a GBS patient. These results, which show a relationship between levels of complement-fixing anti-PNM Ab and the tissue-damaging C5b-9 complex, suggest that peripheral nerve myelin may serve as the target for Ab-mediated complement attack.

Images.

Browse pages

Click on an image below to see the page. View PDF of the complete article

Version history
  • Version 1 (November 1, 1987): No description
Advertisement
Advertisement