These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: [Cellular aspect of neuroinflammation in Guillain-Barré syndrome: a key to a new therapeutic option?].
    Author: Créange A, Sharshar T, Raphaël JC, Gherardi R.
    Journal: Rev Neurol (Paris); 2002 Jan; 158(1):15-27. PubMed ID: 11938319.
    Abstract:
    Guillain-Barré syndrome (GBS) is an acute inflammatory demyelinating neuropathy associated with long-lasting morbidity and substantial risk of mortality. The two reference treatments (plasma exchange-PE and intravenous immunoglobulins-IVIGs) do not change the functional prognosis in patients with very severe disease. Pathogenesis of GBS associates recently characterized humoral and cellular immune dysfunctions. Antibodies against nerve antigens may participate in complement activation, antibody-dependent macrophage cytotoxicity, and reversible conduction failure. Cellular immune reaction is associated with an increase of proinflammatory cytokines (for exemple TNF-alpha), a decrease of anti-inflammatory cytokines (such as TGF-B1), an increase of matrix metalloproteinases (MMP-9-gelatinase B), all abnomalities favoring adhesion to and transmigration across endothelium of immune cells, a key phenomenon in GBS. Recovery of GBS is characterized by the normalization of these abnormalities. Experimental allergic neuritis (EAN), the experimental model of GBS has strikingly similar immunological abnormalities. The treatments of GBS, PE and IVIGs, mainly target the humoral component of the immune response. IFN-B is a cellular immunomodulator that inhibits antigen presentation, TNF-alpha production and binding, modulates macrophages properties. IFN-B increases anti-inflammatory T cell functions and cytokines, such as TGF-B1. IFN-B has important properties on leukodiapedesis by modulating expression of cell adhesion molecules and the MMP-9 proteinase. IFN-B has been used with success in EAN, in some patients with acute exacerbation of chronic inflammatory demyelinating polyneuropathy, and in one patient with GBS. Pathophysiology of GBS, IFN-B properties, and experimental studies support the initiation of a trial of IFN-B in GBS.
    [Abstract] [Full Text] [Related] [New Search]