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Antibody responses to peptides of peripheral nerve myelin proteins P0 and P2 in patients with inflammatory demyelinating neuropathy
  1. H R Inglis1,
  2. P A Csurhes1,
  3. P A McCombe1,2
  1. 1Neuroimmunology Research Centre, The University of Queensland, Brisbane, Queensland, Australia
  2. 2Department of Neurology, Royal Brisbane and Women’s Hospital, Brisbane, Australia; Wesley Research Institute, Wesley Hospital, Brisbane, Australia
  1. Correspondence to:
 Dr P A McCombe
 Department of Medicine, The University of Queensland, C Floor, Clinical Sciences Building, Royal Brisbane and Women’s Hospital, Herston Q 4029, Brisbane, Queensland, Australia; p.mccombe{at}


Background: Antibodies with reactivity to peripheral nerve myelin have previously been found in the serum, and bound to peripheral nerves of patients with Guillain–Barré syndrome (GBS) and chronic inflammatory demyelinating polyradiculoneuropathy (CIDP).

Aim: To investigate the presence of antibodies reactive to specific peptide sequences within the myelin proteins P0 and P2 in patients with GBS, in patients with CIDP, in healthy controls and in patients with other neuropathies (ON).

Methods: Blood was obtained from 48 patients with GBS, 36 with CIDP, 48 with ON and 38 controls. ELISA was used to detect antibody responses to peptides of the human peripheral myelin proteins P0 and P2. Blood samples were collected from patients with GBS in early, peak and recovery stages of GBS to analyse antibody levels throughout the course of the disease.

Results: Significantly increased total IgG levels were found in patients with GBS compared with other groups. A higher percentage of patients with GBS at the peak of disease had antibody reactivity to P214–25 compared with patients with CIDP and control groups. In patients with GBS and CIDP, the percentages of patients with antibody reactivity to P261–70, and peptides derived from P0, were comparable to the control groups. Although some individual patients with GBS had high titres of reactivity to the peptide antigens tested, most patients with GBS and CIDP had levels of antibody similar to controls.

Conclusion: Our data suggest that increased IgG levels and increased antibody reactivity to P2 14–25 in patients with GBS at the peak of disease may play a contributory role in the disease process in some patients with demyelinating forms of GBS.

  • CIDP, chronic inflammatory demyelinating polyradiculoneuropathy
  • GBS, Guillain–Barré syndrome
  • ON, other neuropathies
  • PBST, phosphate-buffered saline containing 0.05% Tween 20

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  • Funding: This work was supported by the National Health and Medical Research Council of Australia and by the Wesley Research Institute.

  • Competing interests: None.

  • This study was approved by the human research ethics committees of the Royal Brisbane, Princess Alexandra, Mater, Greenslopes Private, and Logan Hospitals, as well as the medical research ethics committee of The University of Queensland.

  • Published Online First 8 December 2006