P2-reactive T cells in inflammatory demyelination of the peripheral nerve

Abstract

Lewis rats immunized with P2 protein, a 14.5-kDa protein of the peripheral nerve myelin, develop experimental allergic neuritis, a paralytic disorder with clinical, histologic, and electrophysiologic features similar to those of human Guillain-Barre syndrome (GBS). T cells reactive to P2 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; however, they may induce inflammation and demyelination in the nerves by production of Th1 cytokines. Th2 cytokines may lead to suppression of the inflammation and eventual recovery. There is no conclusive evidence that P: protein plays a role in the pathogenesis of GBS, with or without association with Campylobacter jejuni; however, studies of the immunopathogenesis of P2 protein-induced experimental allergic neuritis are important for understanding the pathogenesis of inflammatory demyelination in the peripheral nerves, the hallmark of GBS.