ANTIBODY-RESPONSES TO P(0) AND P(2) MYELIN PROTEINS IN GUILLAIN-BARRE-SYNDROME AND CHRONIC IDIOPATHIC DEMYELINATING POLYRADICULONEUROPATHY

Immunisation with the peripheral nerve myelin proteins P0 or P2 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 P0 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 P0, sera from 4/7 of GBS, 3/5 of CIDP, 1/2 of ONP patients and 0/1 of NC subjects reacted with a synthetic P0 peptide representing residues 150-169 from the cytoplasmic portion of the molecule. IgG antibodies to P0 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 P2 protein more commonly than antibodies to P0. 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 P2 protein, only a few reacted with P2 peptides 14-25 or 58-81, but without any consistent pattern of reactivity. We propose that IgM antibodies to P0 may contribute to the demyelination in some cases of GBS and CIDP, whereas the more. common antibodies to P2 may merely be markers of a simultaneous pathogenetic T cell-mediated response.