Neuronal antigens modulate the immune response associated to Experimental autoimmune encephalomyelitis (EAE).

ALICIA L. DEGANO; YANINA DITAMO; GERMAN A. ROTH

Australian Society for Immunology

Año: 2004 vol. 82 p. 17 - 17

p style="MARGIN: 0cm 0cm 10pt" class="MsoNormal">Rats primed with bovine myelin (BM) in complete Freunds adjuvant, develop acute experimental autoimmune encephalomyelitis (EAE). We have previously described that intraperitoneal administration prior to the active induction of the disease of a bovine synaptosomal fraction (BSF) and BM were effective ways of suppressing EAE. We found that both treatments diminish the incidence of the disease and reduced biochemical and histological alterations of the central nervous system (CNS). To characterize this suppression process, in this study we examined the antigen-specific immune response in animals protected from EAE. Lymph node mononuclear cells derived from sick EAE rats, as well as from those protected by BM and BSF, showed strong myelin basic protein (MBP) proliferation. Analysis of the humoral response against MBP showed a significant diminution of IgG2b anti-MBP titres in protected BM and BSF rats in