Cell Death Differ:上海生科院揭示IL-12p40在干细胞骨修复中的作用机制

2016-12-30 上海生命科学研究院 上海生命科学研究院

IL-12p40在干细胞骨修复中的作用机制7月29日,国际学术期刊《细胞死亡与分化》(Cell Death & Differentiation)在线发表了中国科学院上海生命科学研究院/上海交通大学医学院健康科学研究所戴尅戎研究组题为IL-12p40 impairs mesenchymal stem cell-mediated bone regeneration via CD4+ T cel

IL-12p40在干细胞骨修复中的作用机制

7月29日,国际学术期刊《细胞死亡与分化》(Cell Death & Differentiation)在线发表了中国科学院上海生命科学研究院/上海交通大学医学院健康科学研究所戴尅戎研究组题为IL-12p40 impairs mesenchymal stem cell-mediated bone regeneration via CD4+ T cells 的最新研究成果,博士研究生徐佳佳等在中国工程院院士戴尅戎及研究员张晓玲的指导下,揭示了IL-12p40在干细胞骨修复中的作用机制。

炎症是骨再生的重要调节因素。炎症反应在骨折损伤后启动,适当的炎症反应可以促进成骨,对于骨折愈合起重要作用。但是,外伤感染或生物材料引起的剧烈、长期的炎症反应会延迟骨修复或导致骨修复失败。因此,阐明促炎因子和骨髓间充质干细胞(bone marrow derived mesenchymal stem cells, BMMSCs)之间的关系是骨免疫学领域的一个重要目标,靶向调控可以有效地促进临床BMMSCs介导的骨修复和再生。

博士研究生徐佳佳等研究发现骨折损伤局部高表达的IL-12和IL-23会损害骨修复,而在缺失T细胞的裸鼠中IL-12和IL-23则不会影响骨再生。研究进一步揭示,IL-12和IL-23通过CD4+ T细胞上调IFN-γ和IL-17,间接抑制BMMSCs成骨分化。具体机制为IL-17可以协同促进IFN-γ诱导的BMMSCs凋亡,体内抑制IL-12和IL-23可以减少BMMSCs凋亡,促进骨再生修复。

该研究发现骨修复过程中关键的炎症调节因子,阐明IL-12和IL-23损害骨再生的具体机制,进一步明确了IL-12p40作为治疗靶点的可行性,为临床骨不愈合等难题提供了一个有效的治疗手段和方法。

此项课题研究获得国家自然科学基金委、上海市科委、上海市卫生和计划生育委员会、上海市教委重点学科建设基金的资助。

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    2017-08-08 axin020
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    2017-10-26 isabellayj
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    2017-08-08 维他命
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    2017-01-01 jjjiang0202
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    2017-01-01 cy0328

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