生物材料异物反应所形成的纤维化胶原囊能够影响甚至阻断材料与组织间的信号传递，导致材料生物学功能的降低甚至完全丧失。目前，纳米纤维支架材料由于能够模拟细胞外基质的结构与功能，在组织工程与药物递送领域中具有良好的应用前景。然而，其超高的比表面积能够明显增加材料与组织界面的非特异性蛋白吸附进而导致异物反应的加强。本研究旨在利用生物学手段调控巨噬细胞的促炎症M1与促愈合M2型功能可塑性来降低纳米纤维与组织界面的异物反应。申请者拟采用免疫调节因子白介素-4(IL-4)，或促免疫抑制型间充质干细胞,或将以上两者相结合,通过自组装与点击化学等技术构建表面功能化纳米纤维支架，探索其调节巨噬细胞功能可塑性转化的效应与协同效应，进而抑制材料与组织界面的异物反应并促进组织再生。本项目将结合生物学、化学与材料学因素构建新颖的功能性免疫抑制型纳米纤维支架，为改善与解决生物材料的异物反应提供新的实验与理论依据。

The process of foreign body reactions lead to contribute the formation of fibrosis collagen capsules and block signal transmission between biomaterials and tissue, which resulting in biomaterials reduce or even completely loss biological functions. Recently, nanofibrous scaffolds have enormous potential for tissue engineering and drug delivery applications since they can mimic the structure and function of native extracellular matrix. However, the large surface area give nanofibrous scaffolds high non-specific protein adsorption, resulting in the enhancement of foreign body reaction. This study aims to use biological tools to regulate pro-inflammatory M1 and pro-wound healing M2 type functional plasticity of macrophage to ease the foreign body reaction of nanofibrous scaffold-tissue interface. Through the use of immunomodulatory cytokines interleukin-4 (IL-4) and pro-immunosuppressive mesenchymal stem cells (MSCs), or combination of above-mentioned two factors, the applicants want to employ layer-by-layer self-assembly and click chemistry techniques to fabricate surface functional three-dimensional nanofibrous scaffold, exploring their effects or synergistic effects on macrophage functional plasticity, further suppressing the foreign body reaction of biomaterial-tissue interface and promoting tissue regeneration. This project will combine biology, chemistry and materials science for the design of new functional immunosuppressive nanofibrous scaffold, which will provide new experimental and theoretical basis to improve and solve the foreign body reactions of biomaterials.