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The Proximal Peripheral Nervous System is a Major Site of Demyelination in Experimental Autoimmune Encephalomyelitis Induced in the Lewis Rat by a Myelin Basic Protein-specific T Cell Clone

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Specialty Neurology
Date 1995 Jan 1
PMID 7545859
Citations 8
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Abstract

Experimental autoimmune encephalomyelitis (EAE) was induced in the Lewis rat by the passive transfer of a cytotoxic CD4+ T cell clone specific for the 72-89 peptide of guinea-pig myelin basic protein (MBP). Histological studies on rats with neurological signs showed that inflammation was present in the proximal peripheral nervous system (PNS), namely the spinal roots, as well as in the central nervous system (CNS). The main sites of demyelination were the spinal roots in the PNS, and the spinal cord root entry and exit zones in the CNS. The major involvement of the proximal PNS in autoimmune disease directed at MBP is in marked contrast to EAE induced by immunisation with myelin proteolipid protein, where the inflammation and demyelination are restricted to the CNS. These findings may have implications for the human inflammatory demyelinating diseases including multiple sclerosis, in which MBP is a putative target antigen.

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References
1.
Pender M, Nguyen K, Willenborg D . Demyelination and early remyelination in experimental allergic encephalomyelitis passively transferred with myelin basic protein-sensitized lymphocytes in the Lewis rat. J Neuroimmunol. 1989; 25(2-3):125-42. DOI: 10.1016/0165-5728(89)90130-6. View

2.
Pender M . Demyelination of the peripheral nervous system causes neurologic signs in myelin basic protein-induced experimental allergic encephalomyelitis. Implications for the etiology of multiple sclerosis. Ann N Y Acad Sci. 1988; 540:732-4. DOI: 10.1111/j.1749-6632.1988.tb27229.x. View

3.
Waxman S . Peripheral nerve abnormalities in multiple sclerosis. Muscle Nerve. 1993; 16(1):1-5. DOI: 10.1002/mus.880160102. View

4.
Hemachudha T, Griffin D, Giffels J, Johnson R, Moser A, Phanuphak P . Myelin basic protein as an encephalitogen in encephalomyelitis and polyneuritis following rabies vaccination. N Engl J Med. 1987; 316(7):369-74. DOI: 10.1056/NEJM198702123160703. View

5.
Olsson Y . Topographical differences in the vascular permeability of the peripheral nervous system. Acta Neuropathol. 1968; 10(1):26-33. DOI: 10.1007/BF00690507. View