SLE患者易发生狼疮性肾炎（LN）。已知 MDSCs在区域炎性反应和免疫耐受的平衡与转化中发挥重要作用。我们前期对不同分期LN患者的肾脏淋巴细胞分群分析发现，MDSCs随着LN进程而大量扩增，提示MDSCs参与LN肾脏的区域免疫调控。但迄今MDSCs在肾脏微环境中扩增机制以及免疫调控作用尚不清。已报道PTEN可负调控PI3K/Akt通路影响MDSCs的扩增与功能，而PTEN启动子区域的超甲基化可导致PTEN表达下调，引起MDSC的NOX激活。有趣的是，我们发现LN患者显著增加的IFNα能下调PTEN的表达，促进MDSC的扩增和NOX的激活。我们推测IFNα可能引起LN患者中PTEN启动子区域超甲基化导致PTEN下调，激活PI3K/Akt通路及NOX的激活参与MDSCs的扩增及免疫功能。故本研究将揭示IFNα调控肾脏微环境中MDSCs分化及功能紊乱的机制，以便提出治疗LN的新策略。

SLE is an autoimmune disorder with diverse clinical manifestations. However, lupus nephritis is the most common character in SLE patients, and lupus nephritis develops in over 60% of adult SLE patients and is even more in children. The regulation of MDSCs in autoimmune diseases has been well defined. In our previous study, we found MDSCs were expanded in different stages of kidney of patients with LN, and this suggested that MDSCs played a role in the progress of LN. The phosphatase and tensin homolog (PTEN) suppress the activity of the PI3K pathway and the PI3K pathway take part in expansion and function of MDSCs. The promoter hypermethylation of PTEN can lead to PTEN down-regulation. PTEN down-regulation can activate NADPH oxidase (NOX), and the activation of NOX promote ROS release. Interestingly, we found IFNα can decrease the expression in LN patients, and promote MDSCs expandsion and NOX activation. We conclude that IFNα may induce promoter hypermethylation of PTEN and this progress lead to PTEN down-regulation in LN patients. This study will clarify the mechanism that how IFNα affect the expression of PTEN and how IFNα enhance the function and expansion of MDSCs. This study will provide a new theory for understanding the role of in the pathogenesis of LN.