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P2 protein-induced experimental allergic neuritis. An ultrastructural study
Journal of the Neurological Sciences
|December 1, 1983
Summary
Experimental allergic neuritis (EAN) induced by P2 protein shows widespread demyelination in spinal nerves. This contrasts with experimental allergic encephalomyelitis (EAE), highlighting P2 protein
Area of Science:
- Neuroimmunology
- Pathology
Background:
- Experimental allergic neuritis (EAN) is an autoimmune model of demyelinating polyneuropathy.
- P2 protein and peripheral nervous system (PNS) myelin are known encephalitogenic antigens.
Purpose of the Study:
- To investigate the demyelinative lesions induced by P2 protein in Lewis rats.
- To compare P2-induced EAN with PNS myelin-induced EAN and experimental allergic encephalomyelitis (EAE).
Main Methods:
- Induction of EAN in Lewis rats using purified bovine P2 protein and PNS myelin.
- Light and electron microscopic examination of neural tissues.
Main Results:
- P2-induced EAN exhibited demyelinative lesions in spinal ganglia and root nerves, affecting both small and large myelinated fibers.
- Lesions included lymphocytic infiltration and myelin sheath dissolution with phagocytic cell invasion.
- P2-induced EAN showed milder disease, more frequent myelin dissolution, and intramyelinic edema compared to PNS myelin-induced EAN.
- Significant demyelination in P2-induced EAN contrasted with minimal myelin changes in EAE induced by myelin basic protein.
Conclusions:
- P2 protein induces significant demyelination in the spinal cord and peripheral nerves, affecting various fiber sizes.
- The pattern of demyelination in P2-induced EAN differs from EAE, suggesting distinct pathogenic mechanisms.
- P2 protein is a potent inducer of demyelinating lesions in the nervous system.