Center for Craniofacial Molecular Biology, Ostrow School of Dentistry, University of Southern California, 2250 Alcazar Street, CSA 103, Los Angeles, CA 90033, USA.
J Dent Res. 2012 Oct;91(10):948-54. doi: 10.1177/0022034512458690. Epub 2012 Aug 17.
Dental pulp stem cells (DPSCs) possess immunoregulatory properties, but the underlying mechanism is not fully understood. Here we showed that DPSCs were capable of inducing activated T-cell apoptosis in vitro and ameliorating inflammatory-related tissue injuries when systemically infused into a murine colitis model. Mechanistically, DPSC-induced immunoregulation was associated with the expression of Fas ligand (FasL), a transmembrane protein that plays an important role in inducing the Fas apoptotic pathway. Knockdown of FasL expression by siRNA in DPSCs reduced their capacity to induce T-cell apoptosis in vitro and abolished their therapeutic effects in mice with colitis. However, the expression level of FasL did not affect either DPSC proliferation rate or multipotent differentiation potential. In summary, FasL governs the immunoregulatory property of DPSCs in the context of inducing T-cell apoptosis.
牙髓干细胞（DPSCs）具有免疫调节特性，但其中的作用机制尚未完全阐明。本研究表明，DPSCs 可在体外诱导活化 T 细胞凋亡，并在系统性输注至结肠炎小鼠模型后减轻炎症相关的组织损伤。机制上，DPSC 诱导的免疫调节与 Fas 配体（FasL）的表达有关，FasL 是一种在诱导 Fas 凋亡途径中起重要作用的跨膜蛋白。DPSCs 中 FasL 的表达被 siRNA 敲低后，其在体外诱导 T 细胞凋亡的能力降低，并且在结肠炎小鼠中丧失了治疗效果。然而，FasL 的表达水平并不影响 DPSCs 的增殖率或多能分化潜能。综上所述，FasL 调控了 DPSCs 在诱导 T 细胞凋亡过程中的免疫调节特性。
