PubMed:18303055 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PubMed/sourceid/18303055","sourcedb":"PubMed","sourceid":"18303055","source_url":"http://www.ncbi.nlm.nih.gov/pubmed/18303055","text":"Roles of complex gangliosides in the development of experimental autoimmune encephalomyelitis.\nWe induced experimental autoimmune encephalomyelitis (EAE) in GM2/GD2 synthase knockout mice (GM2/GD2-/-), which cannot synthesize complex gangliosides, such as GM1, GD1a, GD1b, GT1b, and GQ1b, to investigate the roles of complex gangliosides in the pathogenesis of this disease. We used myelin-oligodendrocyte glycoprotein (MOG) as an immunogen. In active immunization EAE, the severity of clinical score was not different but the disease onset was significantly delayed in GM2/GD2-/- compared with those in wild-type mice. When we transferred MOG-reactive T cells from GM2/GD2-/- or wild-type mice to wild-type mice, no significant differences were observed between the two groups. In contrast, when we transferred MOG-reactive T cells from wild-type mice to GM2/GD2-/- or to wild-type mice, the onset of EAE in GM2/GD2-/- mice was delayed. The recall response of MOG-specific T cells, the function of antigen presenting cells, or the expression of several adhesion molecules in the endothelium were not significantly different between GM2/GD2-/- and wild-type mice. On the other hand, quantitative analysis of cellular infiltration in the central nervous system (CNS) on day 9 of active immunization EAE showed that the CD4+ cell number in the CNS isolated from GM2/GD2-/- mice was significantly less than that from wild-type mice. It indicated that the delayed onset of EAE in GM2/GD2-/- mice was due to the delay of the migration of pathogenic T cells into the CNS. Thus, the complex gangliosides may be involved in the T cell-endothelial cell interaction in the pathogenetic process of 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