作者: Maria Blomqvist , Sara Rhost , Susann Teneberg , Linda Löfbom , Thomas Østerbye
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摘要: The glycosphingolipid sulfatide (SO3-3Galβ1Cer) is a demonstrated ligand for subset of CD1d-restricted NKT cells, which could regulate experimental autoimmune encephalomyelitis, murine model multiple sclerosis, as well tumor immunity and hepatitis. Native mixture isoforms, i.e. molecules with different long-chain bases fatty acid chain lengths saturation. Here, we demonstrate that sulfatide-specific hybridomas recognized several isoforms. These included the physiologically relevant isoforms C24:1 C24:0, major constituents myelin sheet nervous system, C16:0, prominent in pancreatic islet β-cells. most potent isoform was lysosulfatide (lacking acid). Shortened length (C24:1 versus C18:1), or saturation long (C24:0), resulted reduced stimulatory capacity, hydroxylation abolished response. Moreover, not responsible natural autoreactivity toward splenocytes by XV19 T hybridoma cells. Our results reveal promiscuity recognition NKT-cell clone, suggest sulfatide, component β-cells, one ligands type II