Skip Navigation

This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (11)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Kwa, M. S. G.
Right arrow Articles by Baas, F.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kwa, M. S. G.
Right arrow Articles by Baas, F.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Brain, Vol. 126, No. 2, 361-375, February 2003
© 2003 Guarantors of Brain
doi: 10.1093/brain/awg030

Autoimmunoreactivity to Schwann cells in patients with inflammatory neuropathies

Marcel S. G. Kwa1, Ivo N. van Schaik1, Rosalein R. De Jonge1, Anneke Brand2, Luba Kalaydjieva4, Nico van Belzen3, Marinus Vermeulen1 and Frank Baas1

1 Department of Neurology, Academic Medical Centre, University of Amsterdam, 2 Department of Immunohaematology, Leiden University Medical Centre, 3 DMV International, Wageningen, The Netherlands and 4 Western Australian Institute for Medical Research, University of Western Australia, Nedlands, Australia

Correspondence to: Marcel S. G. Kwa, PhD, K2 Room 219, Neurogenetics Laboratory, Department of Neurology, Academic Medical Center, University of Amsterdam, PO Box 22660, 1100 DD Amsterdam, The Netherlands E-mail: m.s.kwa{at}amc.uva.nl

Inflammatory demyelinating neuropathies are characterized by a loss of peripheral nerve myelin. Myelin breakdown is thought to result from an autoimmune reaction towards nerve components. Schwann cells play a crucial role in the synthesis and maintenance of peripheral nerve myelin. An immune attack targeting Schwann cells could therefore affect myelin integrity, leading to disease. We studied the reactivity of sera from patients with Guillain–Barré syndrome (GBS) and chronic inflammatory demyelinating polyneuropathy (CIDP) towards Schwann cells using immunofluorescence microscopy. We found 24% of the GBS (56 out of 233) and 26% of the CIDP (12 out of 46) patients to have circulating immunoglobulin G autoantibodies against proliferating, non-myelinating human Schwann cells. In contrast, healthy donors showed positive staining in only two out of 34 sera. No reaction was found with sera from patients with non-inflammatory neurological disorders. Immunofluorescence was localized at the distal tips (leading lamella) of the Schwann cell processes. Distal tips of neurites (nerve-growth-cones) of in vitro differentiated non-myelinated hNT2 neurons also stained strongly. GBS and CIDP serum immunoreactivity was also observed in teased nerve fibre preparations. These data suggest that, at least part of the immunoreactivity is not directed against myelin, but towards non-myelin proteins and epitopes possibly involved in Schwann cell–axon interaction.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 NEJMHome page
H. Koller, B. C. Kieseier, S. Jander, and H.-P. Hartung
Chronic Inflammatory Demyelinating Polyneuropathy
N. Engl. J. Med., March 31, 2005; 352(13): 1343 - 1356.
[Full Text] [PDF]

Home page
 Hum Mol GenetHome page
R. R. de Jonge, I. N. van Schaik, J. P. Vreijling, D. Troost, and F. Baas
Expression of complement components in the peripheral nervous system
Hum. Mol. Genet., February 1, 2004; 13(3): 295 - 302.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.