Skip to main content
padlock icon - secure page this page is secure

IMMUNOHISTOCHEMICAL LOCALIZATION OF CYTOKINES, C5B-9 AND ICAM-1 IN PERIPHERAL NERVE OF GUILLAIN-BARRE SYNDROME

Buy Article:

The full text article is temporarily unavailable.

We apologise for the inconvenience. Please try again later.

The spectrum of the Guillain-Barre Syndrome (GBS) has recently been widened by the newly identified forms of acute motor axonal neuropathy (AMAN) and acute motor sensory axonal neuropathy (AMSAN). An important question has been raised regarding the possibility for the axon to be a target in immune-mediated damage. Although myelin breakdown is the characteristic feature of classic acute inflammatory demyelinating polyradiculoneuropathy (AIDP), axonal degeneration may occasionally be observed in this form, especially in cases with explosive onset and severe clinical course. Immunohistochemical findings of five frozen sural nerves biopsies of patients with GBS (AIDP variant) tested with a panel of monoclonal antibodies raised against different molecules implicated in immune-mediated processes have principally disclosed an immunoreactivity of tumor necrosis factor-alpha (TNF-alpha) on both Schwann cell membranes and in myelinated and unmyelinated axons. On the other hand, interleukin 1-beta (IL1-beta) labeled Schwann cells, endothelial cells and macrophages; interferon-gamma (IFN-gamma) was observed both in endothelial cells and lymphocytes. Membrane attack complex (C5b-9) deposits were observed on Schwann cell membranes and finally intercellular adhesion molecule-1 (ICAM-1) was localized both on endothelial cells and macrophages. Our findings strongly suggest that TNF-alpha is an important factor in the cascade of events leading to immune-mediated demyelination and axonal damage in GBS.
No References
No Citations
No Supplementary Data
No Article Media
No Metrics

Document Type: Abstract

Affiliations: Journal of the Neurological Sciences 174: 16–21, 2000. Reprinted with permission from Elsevier Science BV.

Publication date: December 1, 2000

  • Access Key
  • Free content
  • Partial Free content
  • New content
  • Open access content
  • Partial Open access content
  • Subscribed content
  • Partial Subscribed content
  • Free trial content
Cookie Policy
X
Cookie Policy
Ingenta Connect website makes use of cookies so as to keep track of data that you have filled in. I am Happy with this Find out more