Lee Eun Mi, Hurh Sunghoon, Cho Bumrae, Oh Kook-Hwan, Kim Seung U, Surh Charles D, Sprent Jonathan, Yang Jaeseok, Kim Jae Young, Ahn Curie
Stem Cell Res Ther. 2013 May 21;4(3):56. doi: 10.1186/scrt206.
Neural stem cells (NSCs) are among the most promising candidates for cell replacement therapy in neuronal injury and neurodegenerative diseases. One of the remaining obstacles for NSC therapy is to overcome the alloimmune response on NSCs by the host.
To investigate the mechanisms of immune modulatory function derived from the interaction of human NSCs with allogeneic T cells, we examined the immune regulatory effects of human NSCs on allogeneic T cells in vitro.
Significantly, NSCs induced apoptosis of allogeneic T cells, in particular CD4+ T cells. Interaction of CD70 on NSCs and CD27 on CD4(+) T cells mediated apoptosis of T cells. Thus, blocking CD70-CD27 interaction prevented NSC-mediated death of CD4(+) T cells.
We present a rational explanation of NSC-induced immune escape in two consecutive stages. First, CD70 constitutively expressed on NSCs engaged CD27 on CD4(+) T cells, which induced Fas ligand expression on CD4(+) T cells. Second, CD4(+) T-cell apoptosis was followed by Fas-Fas ligand interaction in the CD4(+) T cells.
神经干细胞（NSCs）是神经元损伤和神经退行性疾病细胞替代疗法中最有前景的候选者之一。NSC疗法剩下的障碍之一是克服宿主对NSCs的同种免疫反应。
为了研究人NSCs与同种异体T细胞相互作用产生的免疫调节功能机制，我们在体外检测了人NSCs对同种异体T细胞的免疫调节作用。
值得注意的是，NSCs诱导同种异体T细胞凋亡，尤其是CD4+ T细胞。NSCs上的CD70与CD4(+) T细胞上的CD27相互作用介导了T细胞凋亡。因此，阻断CD70-CD27相互作用可防止NSC介导的CD4(+) T细胞死亡。
我们对NSC诱导的免疫逃逸在两个连续阶段进行了合理的解释。首先，NSCs上组成性表达的CD70与CD4(+) T细胞上的CD27结合，诱导CD4(+) T细胞上Fas配体表达。其次，CD4(+) T细胞凋亡后，CD4(+) T细胞中发生Fas-Fas配体相互作用。
