Guillain-Barre syndrome (GBS), an autoimmune post-infectious disorder, is a frequent cause of acute flaccid paralysis in the post-polio era. Recently, two major types of GBS have been described: acute inflammatory demyelinating polyneuropathy (AIDP) characterized by lymphocytic inflammatory demyelination; and acute motor axonal neuropathy (AMAN) characterized by noninflammatory axonal degeneration of motor nerves. Both forms can be associated with preceding infections with Campylobacter jejuni. The immunopathology in these two forms is quite different. In AMAN the initial immunological attack is at the node of Ranvier of motor axons and appears to be associated with antibodies against GD1a ganglioside; in AIDP it is at the external membrane of the Schwann cell. Our studies suggest that molecular mimicry , in which a shared epitope on C. jejuni induces an autoimmune response against nerve, may play an important role in the pathogenesis of GBS. Types of GBS that develop may be influenced by several factors including 1) Anti- glycoconjugate antibody production; 2) Chemokine production; 3) Neuritogenic factors on Campylobacter, 4) Host factors. In this study, the molecular mimicry hypothesis and the factors that may influence the pathogenesis will be evaluated.
Aims are designed to 1) study the role of antiglycoconjugate antibody in AMAN and AIDP; 2) localize the relevant epitopes on motor nerves; 3) study the pattern of chemokine production AMAN and AIDP; 4) determine the bacterial factors that may influence the development of GBS and demonstrate the relevant epitopes; 5) study HLA class I and II haplotypes in AMAN and AIDP.
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