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Antibody responses to P-O and P-2 myelin proteins in Guillain-Barre syndrome and chronic idiopathic demyelinating polyradiculoneuropathy



Antibody responses to P-O and P-2 myelin proteins in Guillain-Barre syndrome and chronic idiopathic demyelinating polyradiculoneuropathy



Journal of Neuroimmunology 46(1-2): 245-251



Immunization with the peripheral nerve myelin proteins P-0 or P-2 induces inflammatory neuropathy in animals. We sought antibodies with an ELISA to these proteins in 38 patients with acute Guillain-Barre syndrome (GBS), 32 patients with chronic idiopathic demyelinating polyradiculoneuropathy (CIDP), 31 patients with other neuropathies (ONP) and 26 normal control (NC) subjects. We discovered IgM antibodies to human P-0 protein in the sera of 18.5% of the patients with GBS, 15.6% with CIDP, 6.4% with ONP and 3.8% of NC subjects. Of the sera which reacted with P-0, sera from 47 of GBS, 35 of CIDP, 12 of ONP patients and 0/1 of NC subjects reacted with a synthetic P-0 peptide representing residues 150-169 from the cytoplasmic portion of the molecule. IgG antibodies to P-0 were slightly less common than IgM antibodies, being present in only 7.9% of GBS, 0% of CIDP and 3% of ONP patients and 0% of NC subjects. We found antibodies to bovine P-2 protein more commonly than antibodies to P-0. IgM antibodies were present in 39.5% of GBS, 34.4% of CIDP, 16.1% of ONP patients and 15.4% of NC subjects. IgG antibodies were present in 18.4% of GBS 12.5% of CIDP, 3.2% of ONP patients and 7.6% of NCs. Of the sera which contained antibodies to P-2 protein, only a few reacted with P-2 peptides 14-25 or 58-81, but without any consistent pattern of reactivity. We propose that IgM antibodies to P-0 may contribute to the demyelination in some cases of GBS and CIDP, whereas the more common antibodies to P-2 may merely be markers of a simultaneous pathogenetic T cell-mediated response.

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Accession: 008170549

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PMID: 7689591


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