Moesin is a possible target molecule for cytomegalovirus-related Guillain-Barré syndrome
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Abstract
Objective: Previous histochemical studies in the demyelinating form of Guillain-Barré syndrome (GBS), acute inflammatory demyelinating polyneuropathy (AIDP), have shown complement deposition on the surface of Schwann cells, and therefore unknown epitopes would be present on the outer surface of Schwann cells.
Methods: We used a proteomic-based approach to search for the target molecules of AIDP in the extracted proteins from schwannoma cells. Sera were obtained from 40 patients with GBS, 31 controls with inflammatory disease, and 46 normal controls.
Results: We found that patients with AIDP after cytomegalovirus (CMV) infection have serum autoantibodies against membrane-organizing extension spike protein (moesin), which is expressed in the Schwann cell processes at the nodes of Ranvier and is crucial for myelination. Of the 40 patients with GBS, 6 had recent CMV infection and 5 of them (83%) had high levels of serum immunoglobulin G antibodies against moesin. The anti-moesin antibodies were found in none of the control subjects with disease including 5 with CMV infection but no neuropathy, and only 2 (4%) of the 46 normal control subjects. Immunocytochemistry showed that moesin was stained at the distal tips of schwannoma cells by sera from the patients with CMV-related AIDP but not by sera from controls.
Conclusion: Moesin is a possible immunologic target molecule of pathogenic autoantibodies in patients with CMV-related AIDP.
Classification of evidence: This study provides Class II evidence that levels of serum anti-moesin antibodies accurately distinguishes CMV-related AIDP from non–CMV-related AIDP (sensitivity 83%, specificity 93%).
GLOSSARY
- AIDP=
- acute inflammatory demyelinating polyneuropathy;
- AMAN=
- acute motor axonal neuropathy;
- CMV=
- cytomegalovirus;
- GBS=
- Guillain-Barré syndrome;
- Ig=
- immunoglobulin;
- MS=
- multiple sclerosis;
- 2-DE=
- 2-dimensional electrophoresis
Footnotes
Go to Neurology.org for full disclosures. Funding information and disclosures deemed relevant by the authors, if any, are provided at the end of the article.
Editorial, page 106
Supplemental data at Neurology.org
- Received September 10, 2013.
- Accepted in final form February 7, 2014.
- © 2014 American Academy of Neurology
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Letters: Rapid online correspondence
- Re:No evidence that molecular mimicry between cytomegalovirus and moesin causes AIDP
- Setsu Sawai, Assistant Professor, Graduate School of Medicine, Chiba University, Japanssawai@faculty.chiba-u.jp
- Masahiro Mori, Chiba, Japan; Satoshi Kuwabara, Chiba, Japan
Submitted August 06, 2014 - No evidence that molecular mimicry between cytomegalovirus and moesin causes AIDP
- Kazuki Miyaji, Research fellow, National University of Singaporemdckazu@nus.edu.sg
- Nobuhiro Yuki, Singapore
Submitted July 24, 2014 - Re:Is moesin a real target for AIDP?
- Setsu Sawai, Assistant Professor, Department of Neurology, Graduate School of Medicine, Chiba University, Japanssawai@faculty.chiba-u.jp
- Masahiro Mori, Chiba, Japan; Satoshi Kuwabara, Chiba, Japan
Submitted July 08, 2014 - Is moesin a real target for AIDP?
- Kazuki Miyaji, Research fellow, National University of Singaporemdckazu@nus.edu.sg
- Jerome Devaux, Marseille, France; Nobuhiro Yuki, Singapore
Submitted June 27, 2014
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