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Cellular immunity in inflammatory autoimmune neuropathies.

Abstract
Autoimmune demyelinating neuropathies, like Guillain-Barré syndrome (GBS) and chronic inflammatory demyelinating polyneuropathy (CIDP), are characterized by local inflammation and demyelination of peripheral nerves. The therapeutic response to plasma exchange and IVIg points to an important role for humoral factors in the pathogenesis of these autoimmune disorders of the peripheral nervous system (PNS). The similarity of the human disease with its animal model disease experimental autoimmune neuritis (EAN), and the activation of T-cell and macrophage derived cytokines all indicate that cellular immunity is also of relevance. Many of the basic principles in autoimmune inflammatory neuropathies have been learned from studies in EAN which can now be linked to the human disorders. This article summarizes current aspects of cellular immunity in autoimmune demyelinating disorders of the PNS. Better understanding of these cellular immunoregulatory mechanisms may help to develop new therapeutic strategies.
AuthorsM Mäurer, K V Toyka, R Gold
JournalRevue neurologique (Rev Neurol (Paris)) Vol. 158 Issue 12 Pt 2 Pg. S7-15 (Dec 2002) ISSN: 0035-3787 [Print] France
PMID12690655 (Publication Type: Journal Article, Review)
Chemical References
  • Cytokines
  • Vascular Cell Adhesion Molecule-1
  • Intercellular Adhesion Molecule-1
Topics
  • Apoptosis (physiology)
  • Cytokines (immunology)
  • Guillain-Barre Syndrome (immunology)
  • Intercellular Adhesion Molecule-1 (immunology)
  • Macrophages (immunology)
  • Major Histocompatibility Complex (immunology)
  • Peripheral Nerves (immunology, pathology)
  • Polyradiculoneuropathy (immunology)
  • Schwann Cells (immunology)
  • T-Lymphocytes (immunology)
  • Vascular Cell Adhesion Molecule-1 (immunology)

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