作為一類病因復(fù)雜且缺乏有效治療手段的中樞神經(jīng)系統(tǒng)自身免疫疾病，多發(fā)性硬化癥多年來一直困擾著國際醫(yī)療界。我國科學(xué)家最新的一項研究揭示了非編碼小RNA在多發(fā)性硬化癥發(fā)生過程中的新機制。
由中國科學(xué)院上海生命科學(xué)研究院生物化學(xué)與細胞生物學(xué)研究所裴鋼院士領(lǐng)導(dǎo)的研究組及他們的合作者,，在研究中發(fā)現(xiàn)一種非編碼小RNA (miR-326)在多發(fā)性硬化癥病人的CD4+T細胞亞群中特異性上調(diào)。而近年來免疫學(xué)家發(fā)現(xiàn)，人體中的CD4+T細胞亞群的大量誘導(dǎo)及其對病灶部位的主動入侵,，能加速誘發(fā)組織損傷。
研究人員通過多發(fā)性硬化癥的小鼠模型研究進一步證實,，人為提高非編碼小RNA (miR-326)的水平,，會加重小鼠的病情，而抑制非編碼小RNA (miR-326)的水平,，則能顯著減輕小鼠的病情,。
這一研究成果已于10月19日在線發(fā)表在國際著名學(xué)術(shù)期刊《自然·免疫》網(wǎng)絡(luò)版上。業(yè)內(nèi)專家認為,，該項研究不僅揭示了非編碼小RNA在多發(fā)性硬化癥發(fā)生過程中的新機制,，并且為包括多發(fā)性硬化癥在內(nèi)的自身免疫疾病的治療，提供了可借鑒的新策略,。
我國科學(xué)家進行的這項研究,，得到了科技部、國家自然科學(xué)基金,、上海市科委和中國科學(xué)院的資金資助,，相關(guān)研究成果已申請專利。（生物谷Bioon.com）
裴剛院士近期研究成果：
Nature：胰島素耐受/II型糖尿病發(fā)病機制研究
生物谷推薦原始出處：
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.
