Miyamoto Katsuichi
Department of Immunology, National Institute of Neuroscience, NCNP.
Nihon Rinsho. 2003 Aug;61(8):1442-8.
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.
实验性自身免疫性脑脊髓炎(EAE)被视为多发性硬化症的模型,是一种典型的Th1介导的自身免疫性疾病。尽管典型的自然杀伤T(NKT)细胞配体α-半乳糖神经酰胺(α-GC)会使NKT细胞产生干扰素-γ和白细胞介素-4,但这种新型配体,即一种具有截短鞘氨醇链的α-GC类似物,可诱导主要产生白细胞介素-4。一致地,口服这种糖脂会通过NKT细胞产生白细胞介素-4诱导自身免疫性T细胞向Th2偏移,从而导致EAE受到抑制。CD1d缺乏多态性以及小鼠和人类NKT细胞对相同配体的交叉反应表明,用这种配体靶向NKT细胞可能是干预多发性硬化症的一种有吸引力的手段。