Nippon Rinsho. 2003 Aug;61(8):1442-8
Department of Immunology, National Institute of Neuroscience, NCNP.
Experimental autoimmune encephalomyelitis(EAE), regarded as a model of multiple sclerosis, is a prototype Th1-mediated autoimmune disease.
Although a prototype natural killer T(NKT) cell ligand, alpha-galactosylceramide(alpha-GC), would render NKT cells produce both IFN-gamma and IL-4, this novel ligand, an analog of alpha-GC with a truncated sphingosine chain, can induce a predominant production of IL-4.
Consistently, an oral administration of this glycolipid induces Th2 bias of autoimmune T cells via production of IL-4 by NKT cells, leading to suppression of EAE.
The lack of polymorphism of CD1d and cross-reactive response of mouse and human NKT cells to the same ligand would indicate that targeting NKT cells with this ligand may be an attractive means for intervening in multiple sclerosis.