Macrophage-inducing FasL on chondrocytes forms immune privilege in cartilage tissue engineering, enhancing in vivo regeneration.

摘要: To obtain stable outcomes in regenerative medicine, controlling inflammatory reactions is a requirement. Previously, auricular chondrocytes tissue-engineered cartilage have been shown to express factors related immune privilege including Fas ligand (FasL) mice. Since elucidation of mechanism on formed regeneration may contribute suppression excessive inflammation, this study, we investigated the function FasL and induction using mouse subcutaneous model. When cocultured, FasL-dysfunctional mice, C57BL/6JSlc-gld/gld (gld), induced less cell death apoptosis macrophage-like cells, RAW264, compared with C57BL/6 mice (wild), suggesting that could induce macrophages. Meanwhile, viability was hardly affected by cocultured although expression type II collagen decreased, indicating macrophages hamper maturation chondrocytes. Tissue-engineered containing gld exhibited greater infiltration macrophages, accumulation proteoglycan than did wild constructs. Analysis coculture medium identified G-CSF as an inducer chondrocytes, G-CSF-treated showed increased formation after transplantation. The interactions between increase secretion which turn suppress tissue reactions, promoting cartilage. These findings provide scientific insight into autologous chondrocyte transplantation, be applied novel strategy for engineering. Stem Cells 2014;32:1208–1219