Kim Eun-Mi, Manzar Gohar, Zavazava Nicholas
Department of Internal Medicine, Division of Immunology, University of Iowa & VAMC Iowa City, Iowa City, IA, USA.
Predictive Model Research Centre, Korea Institute of Toxicology, Yuseong-gu, Daejeon, Korea.
Immunology. 2017 Jun;151(2):191-197. doi: 10.1111/imm.12722. Epub 2017 Mar 22.
The safety of induced pluripotent stem cells (iPSCs) in autologous recipients has been questioned after iPSCs, but not embryonic stem cells (ESCs), were reported to be rejected in syngeneic mice. This important topic has remained controversial because there has not been a mechanistic explanation for this phenomenon. Here, we hypothesize that iPSCs, but not ESCs, readily differentiate into gamete-forming cells that express meiotic antigens normally found in immune-privileged gonads. Because peripheral blood T cells are not tolerized to these antigens in the thymus, gamete-associated-proteins (GAPs) sensitize T cells leading to rejection. Here, we provide evidence that GAPs expressed in iPSC teratomas, but not in ESC teratomas, are responsible for the immunological rejection of iPSCs. Furthermore, silencing the expression of Stra8, 'the master regulator of meiosis', in iPSCs, using short hairpin RNA led to significant abrogation of the rejection of iPSCs, supporting our central hypothesis that GAPs expressed after initiation of meiosis in iPSCs were responsible for rejection. In contrast to iPSCs, iPSC-derivatives, such as haematopoietic progenitor cells, are able to engraft long-term into syngeneic recipients because they no longer express GAPs. Our findings, for the first time, provide a unifying explanation of why iPSCs, but not ESCs, are rejected in syngeneic recipients, ending the current controversy on the safety of iPSCs and their derivatives.
在有报道称诱导多能干细胞(iPSC)而非胚胎干细胞(ESC)在同基因小鼠中被排斥后,iPSC在自体受体中的安全性受到了质疑。这个重要的话题一直存在争议,因为对此现象尚未有机制上的解释。在这里,我们假设iPSC而非ESC容易分化为表达通常在免疫豁免性腺中发现的减数分裂抗原的配子形成细胞。由于外周血T细胞在胸腺中未对这些抗原产生耐受,配子相关蛋白(GAP)会使T细胞致敏,从而导致排斥反应。在这里,我们提供证据表明iPSC畸胎瘤中表达的GAP而非ESC畸胎瘤中表达的GAP是iPSC免疫排斥的原因。此外,使用短发夹RNA沉默iPSC中“减数分裂的主调节因子”Stra8的表达,导致iPSC排斥反应显著消除,支持了我们的核心假设,即iPSC减数分裂开始后表达的GAP是排斥反应的原因。与iPSC不同,iPSC衍生物,如造血祖细胞,能够长期植入同基因受体,因为它们不再表达GAP。我们的研究结果首次为iPSC而非ESC在同基因受体中被排斥的原因提供了统一的解释,结束了目前关于iPSC及其衍生物安全性的争议。