P2-reactive T cells in inflammatory demyelination of the peripheral nerve.
Publication/Presentation Date
12-1-1997
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-Barré 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 P2 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.
Volume
176 Suppl 2
First Page
160
Last Page
163
ISSN
0022-1899
Published In/Presented At
Rostami A. M. (1997). P2-reactive T cells in inflammatory demyelination of the peripheral nerve. The Journal of infectious diseases, 176 Suppl 2, S160–S163. https://doi.org/10.1086/513794
Disciplines
Business Administration, Management, and Operations | Health and Medical Administration | Management Sciences and Quantitative Methods
PubMedID
9396703
Department(s)
Administration and Leadership
Document Type
Article