Development of regenerative medicine for spinal cord injury in HTLV-1 associated myelopathy

我们研究了体干细胞，以促进再生医学的发展，脊髓损伤的人嗜T细胞性病毒1型（HTLV-1）相关的脊髓病（HAM）。我们研究了HTLV-1对体干细胞的感染性，并使用HAM的动物模型来分析体干细胞作为治疗选择的再生能力。我们将来自HTLV-1感染GFP大鼠的脂肪来源的体干细胞（ASC）移植到GFP阴性的非感染大鼠中，没有观察到感染。然而，当我们在体外分析对人源性ASC的感染性时，我们清楚地观察到感染，这表明ASC可能被HTLV-1感染的风险。我们还尝试通过每2周挑战感染，使用HTLV-1感染的大鼠创建早发性HAM的动物模型;然而，未观察到加速作用。最后，我们分析了导致HAM脊髓病变的主要致病过程，我们证明了星形胶质细胞CXCL 10的过度产生在HAM发病机制中起着重要作用。

We studied somatic stem cells in order to forward the development of regenerative medicine for spinal cord injury in Human T-Lymphotropic Virus Type 1 (HTLV-1) associated myelopathy (HAM). We investigated the infectiousness of HTLV-1 to somatic stem cells and used an animal model for HAM to analyze the regenerative capacity of somatic stem cells as a treatment option. We transplanted adipose derived somatic stem cells (ASCs) from HTLV-1 infected GFP rats into GFP-negative non-infected rats, and no infection was observed. However, when we analyzed the infectiousness to human-derived ASCs in vitro, we clearly observed infection, indicating that there is a risk that ASCs could become infected with HTLV-1. We also attempted to create an animal model of early-onset HAM using HTLV-1 infected rats by challenging the infection every 2 weeks; however, no acceleratory effect was observed. Finally, we analyzed the major pathogenic processes leading to spinal cord lesions in HAM, and we demonstrated that overproduction of CXCL10 from astrocytes plays a major role in HAM pathogenesis.