Neuronal antigens modulate the immune response associated with experimental autoimmune encephalomyelitis

• Published in: Immunology and cell biology 2004-02, Vol.82 (1), p.17-23
• Main Authors: Degano, Alicia L, Ditamo, Yanina, Roth, German A
• Format: Article
• Language: English
• Subjects: Adoptive Transfer; Animals; Antigens - immunology; Cell Division; Encephalomyelitis, Autoimmune, Experimental - immunology; Encephalomyelitis, Autoimmune, Experimental - pathology; Encephalomyelitis, Autoimmune, Experimental - therapy; Female; Immunoglobulin G - immunology; Leukocytes, Mononuclear - cytology; Leukocytes, Mononuclear - immunology; Leukocytes, Mononuclear - transplantation; Myelin Basic Protein - immunology; Neurons - immunology; Rats; Rats, Wistar; Synaptosomes - immunology
• ISSN: 0818-9641; 1440-1711
• DOI: 10.1111/j.1440-1711.2004.01200.x

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 contrast to sick EAE rats whose condition could be related to a diminished anti‐MBP Th1 response. Finally, cells from rats protected by BSF and BM reduced the incidence of EAE when they were adoptively transferred into animals prior to active induction of the disease. These results suggest that a mechanism based on the generation of regulatory cells and immune deviation could account for the EAE suppression mediated by myelin as well as synaptosomal antigens.