Experimental allergic neuritis (EAN) was induced in 2 groups of inbred Lewis rats by sensitization with P2 protein and peripheral nervous system (PNS) myelin, both purified from bovine intradural roots. Light- and electron-microscopic study of P2-induced EAN revealed demyelinative lesions in spinal ganglia and root nerves and less frequently in peripheral nerves and root entry zones. Both small and large myelinated fibers were demyelinated, contradictory to the reported selective binding of anti-P2 antibodies to myelin of large fibers. The early lesions were characterised by perivenular lymphocytic infiltration, and subsequent "dissolution" of myelin sheath was associated with invasion of phagocytic cells. The distribution of demyelinative lesions and patterns of demyelination resembled those of PNS myelin-induced EAN except that the disease was milder and dissolution of myelin and intramyelinic edema were more frequently found in P2-induced EAN. The abundance of demyelination in P2-induced EAN strikes contrast to the scarcity of myelin change in experimental allergic encephalomyelitis (EAE) induced by myelin basic protein immunization.
- Experimental allergic encephalomyelitis
- Experimental allergic neuritis
- Guillain-Barré syndrome
- Myelin basic protein P2 protein
ASJC Scopus subject areas
- Clinical Neurology
- Developmental Neuroscience