Division of Gene Therapy, Research Center for Medical Sciences, The Jikei University School of Medicine, Tokyo, Japan; Department of Pediatrics, The Jikei University School of Medicine, Tokyo, Japan.
Institute of Clinical Medicine and Research, Research Center for Medical Sciences, The Jikei University School of Medicine, Tokyo, Japan.
Mol Genet Metab. 2020 Aug;130(4):262-273. doi: 10.1016/j.ymgme.2020.06.007. Epub 2020 Jun 24.
Mucopolysaccharidosis type II (MPS II) is a lysosomal storage disease (LSD) caused by a deficiency of the iduronate-2-sulfatase (IDS) that catabolizes glycosaminoglycans (GAGs). Abnormal accumulations of GAGs in somatic cells lead to various manifestations including central nervous system (CNS) disease. Enzyme replacement therapy (ERT) and hematopoietic stem cell transplantation (HSCT) are the currently available therapy for MPS II, but both therapies fail to improve CNS manifestations. We previously showed that hematopoietic stem cell targeted gene therapy (HSC-GT) with lethal irradiation improved CNS involvement in a murine model of MPS II which lacks the gene coding for IDS. However, the strong preconditioning, with lethal irradiation, would cause a high rate of morbidity and mortality. Therefore, we tested milder preconditioning procedures with either low dose irradiation or low dose irradiation plus an anti c-kit monoclonal antibody (ACK2) to assess CNS effects in mice with MPS II after HSC-GT. Mice from all the HSC-GT groups displayed super-physiological levels of IDS enzyme activity and robust reduction of abnormally accumulated GAGs to the wild type mice levels in peripheral organs. However, only the mice treated with lethal irradiation showed significant cognitive function improvement as well as IDS elevation and GAG reduction in the brain. These results suggest that an efficient engraftment of genetically modified cells for HSC-GT requires strong preconditioning to ameliorate CNS involvement in cases with MPS II.
黏多糖贮积症 II 型(MPS II)是一种溶酶体贮积病(LSD),由分解糖胺聚糖(GAG)的艾杜糖-2-硫酸酯酶(IDS)缺乏引起。GAG 在体细胞中的异常积累导致各种表现,包括中枢神经系统(CNS)疾病。酶替代疗法(ERT)和造血干细胞移植(HSCT)是目前治疗 MPS II 的方法,但这两种疗法都不能改善 CNS 表现。我们之前的研究表明,针对造血干细胞的基因治疗(HSC-GT)与致死性照射相结合,可改善缺乏 IDS 基因编码的 MPS II 小鼠模型中的 CNS 受累。然而,强烈的预处理,包括致死性照射,会导致高发病率和死亡率。因此,我们测试了较温和的预处理程序,包括低剂量照射或低剂量照射加抗 c-kit 单克隆抗体(ACK2),以评估 MPS II 小鼠在 HSC-GT 后的 CNS 效应。所有 HSC-GT 组的小鼠均表现出超生理水平的 IDS 酶活性,并且在外周器官中异常积累的 GAG 显著减少至野生型小鼠水平。然而,只有接受致死性照射的小鼠表现出认知功能显著改善,以及大脑中的 IDS 升高和 GAG 减少。这些结果表明,为了改善 MPS II 患者的 CNS 受累情况,HSC-GT 的基因修饰细胞的有效植入需要强烈的预处理。