Nature Neuroscience:我国学者提出免疫异常型自闭症的潜在治疗策略

2021-04-19 生物世界 生物世界

孤独症谱系障碍(Autism Spectrum Disorder,简称ASD),是广泛意义上的自闭症,是一组中枢神经系统发育疾病,其致病机制复杂,病因高度异质化,存在巨大的未满足临床需求。

孤独症谱系障碍(Autism Spectrum Disorder,简称ASD),是广泛意义上的自闭症,是一组中枢神经系统发育疾病,其致病机制复杂,病因高度异质化,存在巨大的未满足临床需求。目前学界主要聚焦于其遗传学病因及病理机制,已发现一部分孤独症的发生可归因于数百种遗传异常,缺乏具有普适性的靶点以支撑常规药物研发。

流行病学及实验动物研究结果表明,孕期母体感染病原体所引发的母体免疫激活(MIA)是诱发子代产生孤独症等神经精神疾病的重要风险因素;同时,MIA对子代的外周和中枢神经免疫系统可产生持久性影响,这可能是导致部分免疫异常型孤独症的原因。

2021年4月15日,上海市精神卫生中心-中科院上海药物研究所联合实验室周子凯研究员与南京医科大学生殖医学国家重点实验室、病原生物学系季旻珺教授合作,在神经科学顶级期刊 Nature Neuroscience 在线发表了题为:Rescue of maternal immune activation-induced behavioral abnormalities in adult mouse offspring by pathogen-activated maternal Treg cells 的研究论文。

该研究建立了母体免疫激活(MIA)的新型疾病动物模型,揭示了MIA影响子代免疫系统并造成孤独症相关表型的机制,并发现可以通过调节成年期子代小鼠的免疫系统改善其孤独症的表型。

研究者们首先采用感染全球1/3人口的弓形虫速殖子可溶性抗原(STAg)诱导母体免疫激活(MIA),建立了子代具有免疫异常及孤独症表型的小鼠模型。与学界常用的病毒模拟物poly(I:C)及细菌模拟物脂多糖(LPS)这两种化学物质相比,寄生虫模拟物STAg为复合抗原,可以更全面地诱导免疫谱系异常,特别是可以有效诱发获得性细胞免疫反应。

研究团队发现,子代病鼠直至成年都存在外周及中枢神经免疫谱系异常,其CD4? T细胞谱与部分孤独症患者高度一致;并且病鼠具有社交互动缺陷、重复刻板动作、交流障碍的孤独症核心症状,以及显着的焦虑表型。

弓形虫速殖子复合抗原(STAg)可有效诱导母体免疫激活(MIA)产生疾病高风险的子代小鼠。具有孤独症表型的子代(ASD offspring)与健康子代(Healthy offspring)相比,外周Th1/Th17细胞亚群比例上调,脑内星型胶质细胞(Astrocyte)分泌大量IL-6因子造成脑功能障碍。采用过继性细胞治疗输入外周的Treg细胞在趋化因子CCL22的作用下迁入脑内,通过高表达PD1、ICOS、IL-10等分子调节神经功能,改善病鼠的孤独症相关表型。

对成年病鼠进行过继性调节性T细胞(Treg)治疗后,研究团队发现,虽然病鼠脑白质纤维微结构异常的改善相对有限,但该治疗有效地逆转了绝大部分免疫学和行为学表型。通过单细胞测序技术(scRNA-seq)对比不同来源的Treg细胞的转录组,研究团队鉴定出一组高疗效的Treg细胞亚群及其转录组学特征,这类高疗效的Treg细胞能够更好地迁入与疾病症状关联的脑区起效。

该工作通过构建具有孤独症表型的新型母体免疫激活(MIA)疾病动物模型并进行研究,提出依照高疗效细胞亚群的分子特征进行工程化改造的调节性T细胞药物有望改善免疫异常型孤独症的核心症状,为后续临床转化研究提供了新思路。

据悉,南京医科大学副教授徐志鹏、上海药物所博士后张小云、南京医科大学博士生常浩为本研究的共同第一作者。上海药物所/上海交通大学医学院附属精神卫生中心(兼)周子凯研究员和南京医科大学季旻珺教授为共同通讯作者。该工作获得国家自然科学基金、上海市科学技术委员会、江苏省自然科学基金、上海市精神卫生中心等基金资助。

原始出处:

Xu, Z., Zhang, X., Chang, H. et al. Rescue of maternal immune activation-induced behavioral abnormalities in adult mouse offspring by pathogen-activated maternal Treg cells. Nat Neurosci (2021). https://doi.org/10.1038/s41593-021-00837-1.

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    2021-09-09 liye789132251
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    2021-04-20 lsndxfj
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    2021-04-20 xiongke014

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