自身免疫性葡萄膜炎（AU）是导致视力丧失的主要原因之一，Th17/Treg 细胞亚群的比例失衡在其中发挥了重要作用，但其确切机制尚未阐明。间充质干细胞来源的外泌体（MSCs-exo）具有MSCs的部分生物学特性，可发挥广泛的生物学功能，最新的研究表明其可以调节T细胞亚群分化。我们前期工作发现，在实验性自身免疫性葡萄膜炎（EAU）模型中，MSCs可以通过CD39-CD73-Ado通路与CD4+T淋巴细胞相互作用，营造出免疫抑制微环境；同时，MSCs-exo可以有效调节Th17/Treg细胞失衡，达到治疗作用。因此我们推测，MSCs-exo可能通过其表面CD73与CD4+T细胞表面CD39/CD73共同作用促进Ado生成，进而调节Th17/Treg细胞比例，在EAU中发挥控制炎症的作用。在预实验的基础上，本研究将深入讨论MSCs-exo治疗EAU的相关分子机制，为临床防治AU提供新的思路。

Autoimmune uveitis (AU) is one of the leading causes of vision loss which mainly induced by imbalance of Th17/Treg cells, but the exact mechanism has not yet been elucidated. Mesenchymal stem cell-derived exosomes (MSCs-exo) have partial biological properties of MSCs which can produce a wide range of biological functions, and recent studies have shown that they can regulate T cell subgroup differentiation. Our preliminary work found that, MSCs interacted with CD4+T lymphocytes via the CD39-CD73-adenosine (Ado) pathway to create an immunosuppressive microenvironment in the experimental autoimmune uveitis (EAU) models; MSCs-exo could effectively inhibit the chemotaxis of Th1 and Th17 cells, promote the chemotaxis of Treg cells, which further regulated the imbalance of Th17/Treg cells to achieve therapeutic effects. Therefore, we hypothesized that MSCs-exo could regulat the ratio of Th17/Treg cells in combination with CD4+T cells via CD39/CD73/Ado pathway, exerting the role of controlling inflammation in EAU. On the basis of pre-experiment, this study will be the first to explore the relationship between MSCs-exo, the ratio of Th17/Treg cells and CD39-CD73-Ado pathway in EAU. Our study may provide an important theoretical basis and new inspect for AU treatment.