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

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

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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 Gullain-Barre 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 and 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.

Original languageEnglish (US)
Pages (from-to)1492-1497
Number of pages6
JournalJournal of Clinical Investigation
Volume80
Issue number5
StatePublished - 1987
Externally publishedYes

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Guillain-Barre Syndrome
Complement Membrane Attack Complex
Myelin Sheath
Antibodies
Peripheral Nerves
Paraproteins
Neuritis
Protein S
Demyelinating Diseases
Antigen-Antibody Complex
Serum
Polymerization
Anti-Idiotypic Antibodies
Enzyme-Linked Immunosorbent Assay
Immunohistochemistry
Membranes

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Koski, C. L., Sanders, M. E., Swoveland, P. T., Lawley, T. J., Shin, M. L., Frank, M. M., & Joiner, K. A. (1987). Activation of terminal components of complement in patients with Guillain-Barre syndrome and other demyelinating neuropathies. Journal of Clinical Investigation, 80(5), 1492-1497.

Activation of terminal components of complement in patients with Guillain-Barre syndrome and other demyelinating neuropathies. / Koski, C. L.; Sanders, M. E.; Swoveland, P. T.; Lawley, T. J.; Shin, M. L.; Frank, M. M.; Joiner, Keith A.

In: Journal of Clinical Investigation, Vol. 80, No. 5, 1987, p. 1492-1497.

Research output: Contribution to journalArticle

Koski, C. L. ; Sanders, M. E. ; Swoveland, P. T. ; Lawley, T. J. ; Shin, M. L. ; Frank, M. M. ; Joiner, Keith A. / Activation of terminal components of complement in patients with Guillain-Barre syndrome and other demyelinating neuropathies. In: Journal of Clinical Investigation. 1987 ; Vol. 80, No. 5. pp. 1492-1497.
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