Chen Xi, Zhang Zheng-Yun, Zhou Hao, Zhou Guang-Wen
Department of Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.
Dev Growth Differ. 2014 Apr;56(3):233-44. doi: 10.1111/dgd.12124. Epub 2014 Mar 19.
Infective factors cause the perpetuation of inflammation as a result of the permanent exposure of the immune system to exogenous or endogenous products of virus or bacteria. Mesenchymal stem cells (MSCs) can be exposed to this infective environment, which may change the characteristics and therapeutic potency of these MSCs. MSCs have the ability to repair damaged and inflamed tissues and regulate immune responses. In this study, we demonstrated that MSCs express functional Toll-like receptors (TLR) 3 and 4, the Toll-like receptor families that recognize the signals of viral and bacterial mimics, respectively. The specific stimulations did not affect the self-renewal and apoptosis capabilities of MSCs but instead promoted their differentiation into the adipocytes and osteoblasts with the TLR3 ligand. The reverse of these results were obtained with the TLR4 ligand. The migration of the MSCs to stimulate either of the two specific ligands was inhibited at different times, whereas the immunogenicity and immunosuppressive properties of the MSCs were not weakened unlike in the MSCs group. These results suggest that TLR3 and TLR4 stimulation affect the characterization of MSCs.
感染因素导致炎症持续存在，这是由于免疫系统长期暴露于病毒或细菌的外源性或内源性产物。间充质干细胞（MSC）可能会暴露于这种感染环境中，这可能会改变这些MSC的特性和治疗效力。MSC具有修复受损和发炎组织以及调节免疫反应的能力。在本研究中，我们证明MSC表达功能性Toll样受体（TLR）3和4，这两个Toll样受体家族分别识别病毒和细菌模拟物的信号。特定刺激并未影响MSC的自我更新和凋亡能力，反而通过TLR3配体促进其向脂肪细胞和成骨细胞分化。使用TLR4配体得到了相反的结果。在不同时间，MSC向两种特定配体之一的迁移受到抑制，而与MSC组不同的是，MSC的免疫原性和免疫抑制特性并未减弱。这些结果表明，TLR3和TLR4刺激会影响MSC的特性。
