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

为了促进人类嗜t淋巴病毒1型（HTLV-1）相关脊髓病（HAM）脊髓损伤的再生医学发展，我们研究了体细胞干细胞。我们研究了HTLV-1对体细胞干细胞的传染性，并使用HAM动物模型来分析体细胞干细胞作为治疗选择的再生能力。我们将HTLV-1感染的GFP大鼠的脂肪源性体细胞干细胞（ASCs）移植到GFP阴性的未感染大鼠中，未观察到感染。然而，当我们在体外分析对人源性ASCs的传染性时，我们清楚地观察到感染，表明ASCs可能被HTLV-1感染。我们还尝试用HTLV-1感染的大鼠每2周挑战感染，创建早发性HAM动物模型；然而，没有观察到加速效应。最后，我们分析了导致HAM脊髓病变的主要致病过程，并证明星形胶质细胞过量产生CXCL10在HAM发病中起主要作用。

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.