阻滞IFN-α的产生被认为可缓解SLE的发生及发展。循环的树突状细胞（DCs）主要包括髓系DC（mDC）和浆细胞样DC（pDC），pDC是主要产生IFN-α的细胞。我们前期发现SLE的间充质干细胞（MSC）低表达miR-30a，外源性正常的MSC高表达miR-30a，且能降低DCs表达IFN-α；miR-30a能上调MSC自身的PGE2合成基因COX2的表达，还可靶向IFNAR2。已知PGE2是MSC发挥免疫调节的关键因素，IFNAR2对DCs的IFN-α通路活化至关重要。推测miR-30a可通过PGE2和IFNAR2影响DCs产生IFN-α。可是迄今还不完全清楚miR-30a如何调节MSC产生PGE2？MSC分泌的miR-30a是否通过IFNAR2调控DCs产生IFN-α及其自反馈作用？本研究将探索MSC通过miR-30a调控DCs的机制，提出MSC改善自身免疫病的新理论。

Systemic lupus erythematosus (SLE) is a chronic inflammatory autoimmune disease and characterized by the production of autoantibodies and immune complexes that affects multiple organs. IFN-α plays a significant role in the occurrence and development of SLE and inhibiting the production of IFN-α can relieve the disease conditiion of SLE. Dendritic cells (DCs) is the most powerful professional antigen presenting cell in organism. Many studies have shown that the phenotypic and function of DCs are abnormal in SLE patients and lupus mice. Circulating dendritic cells mainly include myeloid DC (mDC) and plasmacytoid DC (pDC). Over the past two decades, numerous studies have suggested that IFN-α is mainly produced by pDC, but mDC can produce IFN-α too. In our previous study, MSC transplantion can alleviate the disease condition of SLE and reduce the level of IFN-α . MSC can suppress the differentiation and function of DCs. Many studies reported that MSC could secret many soluble factors, among which PGE2 plays a key role in MSC mediated the inhibition of production of IFN-α by DCs. We have found that the expression of miR-30a was lower in MSC of SLE patients than that of healthy people. miR-30a can upregulate the expression of COX2 which can promote the synthesis of PGE2. Also miR-30a can target the 3'UTR of IFNAR2 which is essential for the activition of IFN-I signaling pathway. However the mechanism on MSC regulates the synthesis of PGE2 is still unclear so far. Whether miR-30a secreted by MSC can target the IFNAR2 of DCs? This study will clarify the mechanism that how MSC affect the secretion of IFN-α by DCs via miR-30a and provide new theory for MSC transplantation in the treatment of SLE.