P-2-REACTIVE T-CELLS IN INFLAMMATORY DEMYELINATION OF THE PERIPHERAL-NERVE

Lewis rats immunized with P-2 protein, a 14.5-kDa protein of the perip heral nerve myelin, develop experimental allergic neuritis, a paralyti c disorder with clinical, histologic, and electrophysiologic features similar to those of human Guillain-Barre syndrome (GBS). T cells react ive to P-2 protein or a peptide corresponding to 53-78 residues of the protein can transfer the disease to naive animals. The mechanisms by which these T cells induce demyelination are not well understood; howe ver, they maw induce inflammation and demyelination in the nerves by p roduction of Th1 cytokines. Th2 cytokines may lead to suppression of t he inflammation and eventual recovery. There is no conclusive evidence that P-2 protein plays a role in the pathogenesis of GBS, with or wit hout association with Campylobacter jejuni; however, studies of the im munopathogenesis of P-2 protein-induced experimental allergic neuritis are important or understanding the pathogenesis of inflammatory demye lination in the peripheral nerves, the hallmark of GBS.