EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS - ANTIGEN-INDUCED INHIBITION OF BIOCHEMICAL AND IMMUNOHISTOLOGICAL ALTERATIONS

A comprehensive biochemical, immunological, and histological study was undertaken during suppression of experimental autoimmune encephalomye litis (EAE) induced by antigen-specific inhibition of the immune respo nse, Pretreatment of Wistar rats by intraperitoneal administration of low doses of saline-soluble bovine myelin or myelin basic protein (MBP ) but not with ovalbumin suppresses the appearance of the clinical sym ptoms of EAE induced by sensitization with bovine myelin in complete F reund's adjuvant, Analysis of the central nervous system (CNS) of anim als pretreated with MBP or whole myelin shows inhibition of the diminu tion of MBP and 2',3'-cyclic nucleotide 3'-phosphohydrolase (CNPase) a ctivity observed in the EAE animals or in rats pretreated with ovalbum in, With respect to the CNS lipid content, these suppressive treatment s abolish the increase in esterified cholesterol and partially revert the diminution in the content of cerebrosides and total cholesterol ch aracteristic of the acute stage of the disease, Concomitantly, meninge al and parenchymal infiltration with mononuclear cells and deposits of immunoglobulins in the infiltrated regions as well as in spinal cord motor neurons were reduced, Analysis of the humoral response to myelin antigens shows that all EAE as well as treated animals developed anti bodies to MBP and other myelin proteins, However, a higher incidence a nd level of these antibodies was observed in nontreated EAE animals an d MBP- and ovalbumin-treated rats, while rats treated with total bovin e myelin showed a highly reduced humoral response, The present results indicate that intraperitoneal treatment with soluble forms of myelin antigens, concomitant with the suppression of the clinical symptoms of the disease, markedly reduces the biochemical and histological altera tions occurring in EAE animals and produces changes in the autoimmune humoral response. (C) 1996 Wiley-Liss, Inc.