CLINICAL AND HISTOLOGICAL-FINDINGS IN PROTEOLIPID PROTEIN-INDUCED EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS (EAE) IN THE LEWIS RAT - DISTRIBUTION OF DEMYELINATION DIFFERS FROM THAT IN EAE INDUCED BY OTHER ANTIGENS

Proteolipid protein (PLP) is the major protein of central nervous syst em (CNS) myelin. In some species, intradermal inoculation with PLP and adjuvants causes experimental autoimmune encephalomyelitis (PLP-EAE) characterized by neurological signs of tail and limb weakness and by i nflammation and demyelination in the CNS. A previous study found that inoculation of Lewis rats with 100 mu g of PLP causes PLP-EAE with a l ow incidence of neurological signs and a highly variable clinical cour se. In the present study we assessed PLP-EAE produced by inoculation w ith 1000 mu g of PLP per rat. Fifty-one of 59 (86%) Lewis rats develop ed neurological signs 8 to 20 days (mean = 12.0 +/- 2.0) after inocula tion with 1000 mu g of PLP. In such rats, mononuclear cell infiltrates were present in the brain and spinal cord while primary demyelination occurred mainly in the subpial regions of the spinal cord, especially in the dorsal root entry and ventral root exit zones. The histologica l findings were compared with those in acute EAE induced in the Lewis rat by inoculation with whole CNS tissue or with myelin basic protein: in PLP-EAE, in contrast to these other models, the disease was essent ially restricted to the CNS. This form of EAE should be useful in futu re studies of the consequences of autoimmunity to PLP.