作为一类病因复杂且缺乏有效治疗手段的中枢神经系统自身免疫疾病，多发性硬化症多年来一直困扰着国际医疗界。我国科学家最新的一项研究揭示了非编码小RNA在多发性硬化症发生过程中的新机制。
由中国科学院上海生命科学研究院生物化学与细胞生物学研究所裴钢院士领导的研究组及他们的合作者，在研究中发现一种非编码小RNA (miR-326)在多发性硬化症病人的CD4+T细胞亚群中特异性上调。而近年来免疫学家发现，人体中的CD4+T细胞亚群的大量诱导及其对病灶部位的主动入侵，能加速诱发组织损伤。
研究人员通过多发性硬化症的小鼠模型研究进一步证实，人为提高非编码小RNA (miR-326)的水平，会加重小鼠的病情，而抑制非编码小RNA (miR-326)的水平，则能显著减轻小鼠的病情。
这一研究成果已于10月19日在线发表在国际著名学术期刊《自然·免疫》网络版上。业内专家认为，该项研究不仅揭示了非编码小RNA在多发性硬化症发生过程中的新机制，并且为包括多发性硬化症在内的自身免疫疾病的治疗，提供了可借鉴的新策略。
我国科学家进行的这项研究，得到了科技部、国家自然科学基金、上海市科委和中国科学院的资金资助，相关研究成果已申请专利。（生物谷Bioon.com）
裴刚院士近期研究成果：
Nature：胰岛素耐受/II型糖尿病发病机制研究
生物谷推荐原始出处：
Nature Immunology 18 October 2009 | doi:10.1038/ni.1798
MicroRNA miR-326 regulates TH-17 differentiation and is associated with the pathogenesis of multiple sclerosis
Changsheng Du1,5, Chang Liu1,5, Jiuhong Kang1,2, Guixian Zhao3, Zhiqiang Ye4, Shichao Huang1, Zhenxin Li3, Zhiying Wu3 & Gang Pei1,2
Interleukin 17 (IL-17)-producing T helper cells (TH-17 cells) are increasingly recognized as key participants in various autoimmune diseases, including multiple sclerosis. Although sets of transcription factors and cytokines are known to regulate TH-17 differentiation, the role of noncoding RNA is poorly understood. Here we identify a TH-17 cell–associated microRNA, miR-326, whose expression was highly correlated with disease severity in patients with multiple sclerosis and mice with experimental autoimmune encephalomyelitis (EAE). In vivo silencing of miR-326 resulted in fewer TH-17 cells and mild EAE, and its overexpression led to more TH-17 cells and severe EAE. We also found that miR-326 promoted TH-17 differentiation by targeting Ets-1, a negative regulator of TH-17 differentiation. Our data show a critical role for microRNA in TH-17 differentiation and the pathogenesis of multiple sclerosis.
1 Laboratory of Molecular Cell Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Graduate School of the Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, China.
2 School of Life Science and Technology, Tongji University, Shanghai, China.
3 Department of Neurology and Institute of Neurology, Huashan Hospital, Shanghai Medical College, Shanghai, China.
4 Key Laboratory of Systems Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.
5 These authors contributed equally to this work.
