Suppression of murine experimental autoimmune optic neuritis byinnovation of mature dendritic cells transfected with calcitoningene-related peptide gene

该疾病在具有抗AQP 4抗体以及抗髓鞘少突胶质细胞糖蛋白（MOG）抗体的个体中变得严重。在视神经炎模型中，视力首先下降，小胶质细胞和炎性细胞浸润。此后，轴突数量减少，视觉诱发电位（VEP）潜伏期延长。应用该现象，尝试了使用转染有CGRP的树突状细胞或转染有IL-10的树突状细胞的细胞疗法，并且发现有效抑制视神经炎。与此同时，作为一种更实用的治疗方法，新的多发性硬化症药物芬戈莫德的管理表明抑制细胞浸润到视神经。

The disease becomes severe in individuals who possess anti-AQP4 antibodies, together with anti-myelin oligodendrocyte glycoprotein (MOG) antibodies. In optic neuritis models, visual acuity decreases first, infiltration of microglia andinflammatory cells. Thereafter, the number of axons decreases and latency of visually evoked potential (VEP) is prolonged. Applying this phenomenon, cell therapy using dendritic cells transfected with CGRP or dendritic cells transfected with IL-10 was attempted, and was found to be effective in suppressing optic neuritis. At the same time, as a more practical therapy, administration of the new multiple sclerosis drug fingolimodsuggests suppression of cell infiltration into the optic nerve.