miR-223主要在骨髓细胞表达，调控粒细胞的分化，在癌症和病毒感染中发挥作用。最近，研究发现miR-223在风湿性关节炎和急性白血病人T细胞中高表达，具有预防和治疗相关疾病的作用。但对T细胞介导的多发性硬化症及其动物模型自身免疫性脑脊髓炎（EAE）的调节作用尚不清楚。我们研究发现EAE小鼠脾脏和脊髓中miR-223表达显著升高，并且干扰抑制miR-223后，可显著延缓发病时间并降低疾病临床评分。因此，我们认为miR-223可促进EAE发生发展。本项目拟通过超表达及抑制miR-223表达的稳定细胞系和疾病动物模型，在体内小鼠EAE疾病模型和体外T细胞定向分化中，研究miR-223对实验性自身免疫性脑脊髓炎及其相关辅助T细胞分化的调节作用和分子机制。在整体、细胞和分子水平揭示miR-223调节EAE的作用机理，为人类多发性硬化症以及miR-223相关的自身免疫和炎症性疾病的预防和治疗奠定

MiR-223 is mainly express in bone marrow cell, controlling the differentiation of granulocyte, which plays an important role in cancer and virus infection. Recently study found that miR-223 highly expressed in the T cells of rheumatoid arthritis and human acute leukemia, which has effect on prevention and treatment of the related diseases. But the role of miR-223 in regulating of multiple sclerosis (MS) and experimental autoimmune encephalomyelitis(EAE) mediated by T cells is not clear. Our study found that miR-223 expression significantly increased in the spleen and spinal cord of EAE mice. While, after suppression the expression of miR-223, it can significantly delay the onset time and reduce clinical score. Therefore, our purpose is that miR-223 can promote the development of EAE. The project is proposed to study the regulating role and molecular mechanism of miR-223 on experimental autoimmune encephalomyelitis and related T helper cells differentiation by over expression and inhibition miR-223 expression in stable cell lines and animal model of mice in vivo and in vitro. We aim to reveal the regulation mechanism of miR-223 on EAE mice through the whole-body, cell and molecular level. It will be the foundation for miR-223 to treat human multiple sclerosis and related autoimmune and inflammatory disease.