作者: Jean-Pierre Zanetta
DOI: 10.1016/S0167-7306(08)60298-7
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摘要: Publisher Summary Most human autoimmune demyelinating diseases, glycoproteins, and their carbohydrate moieties involved in myelin adhesion processes are the immunological targets. The exception is lectin cerebellar soluble (CSL), which also these mechanisms by binding glycans of glycoproteins. hypothesis leukocyte CSL as an target multiple sclerosis (MS) suggests new therapies based on glycobiology. suppression experimental allergic encephalomyelitis (EAE) animals after treatments with castanospermine indicates that N-glycans homing activated cells specific endothelial cells. Furthermore, this inhibitor α-1,2-glucosidase has been shown to inhibit activation. Due role activation formation aggregates, it expected intravenous injections low doses will modify preferentially circulating This reduce capacities. Although risks destruction cell junctions including evident, slow turnover junctional glycoproteins may provide a specificity action. Alternatively, structure Man 6 GlcNAc 2 be very efficient aggregation. A similar therapeutical approach could proposed for HNK- 1 epitope.