Journal of Dental Research · 2012 · 147 citations · 23 references
Life SciencesImmunologyApoptosisImmunoregulationInflammationApoptosis ModulationApoptotic SignalingHost Immune ResponseInflammatory SignalingMucosal InflammationPulp Cell BiologyDifferentiation PotentialFas LigandFas Ligand-mediated ApoptosisFas Receptor SignalingImmunomodulatory EffectsImmunoregulatory SignalingInflammatory Tissue DamagePulpal Immune Cells
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.
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