Al-Jaderi Zaidoon, Maghazachi Azzam A
Department of Physiology, Institute of Basic Medical Sciences, Faculty of Medicine, University of Oslo, POB 1103, Oslo N-0317, Norway.
College of Medicine, University of Sharjah, Al-Sharja 27272, UAE.
Toxins (Basel). 2015 Nov 13;7(11):4730-44. doi: 10.3390/toxins7114730.
Experimental autoimmune encephalomyelitis (EAE) is a CD4⁺ T cell mediated inflammatory demyelinating disease that is induced in mice by administration of peptides derived from myelin proteins. We developed EAE in SJL mice by administration of PLP139-151 peptide. The effect of treating these mice with 1α,25-Dihydroxyvitamin D₃ (vitamin D₃), or with monomethyl fumarate (MMF) was then examined. We observed that both vitamin D₃ and MMF inhibited and/or prevented EAE in these mice. These findings were corroborated with isolating natural killer (NK) cells from vitamin D₃-treated or MMF-treated EAE mice that lysed immature or mature dendritic cells. The results support and extend other findings indicating that an important mechanism of action for drugs used to treat multiple sclerosis (MS) is to enhance NK cell lysis of dendritic cells.
实验性自身免疫性脑脊髓炎（EAE）是一种由CD4⁺ T细胞介导的炎症性脱髓鞘疾病，通过给小鼠注射髓磷脂蛋白衍生肽诱导产生。我们通过给SJL小鼠注射PLP139 - 151肽来诱导EAE。然后研究了用1α,25 - 二羟基维生素D₃（维生素D₃）或富马酸单甲酯（MMF）治疗这些小鼠的效果。我们观察到维生素D₃和MMF均能抑制和/或预防这些小鼠的EAE。从经维生素D₃或MMF治疗的EAE小鼠中分离出的自然杀伤（NK）细胞能够裂解未成熟或成熟的树突状细胞，这证实了上述发现。这些结果支持并扩展了其他研究结果，表明用于治疗多发性硬化症（MS）的药物的一个重要作用机制是增强NK细胞对树突状细胞的裂解作用。
