细胞自噬是生命的基本现象。已发现自噬在免疫系统中发挥重要作用。研究提示UVB可以影响细胞的自噬水平。作为影响SLE重要因素，目前尚不清楚UVB是否通过自噬影响SLE。前期我们通过miRNA芯片技术发现：UVB照射SLE患者和正常人外周血单一核细胞（PBMC），不同人群的PBMC照射前后miR-125b会出现明显的差异表达，且预测的其下游靶点存在调控自噬相关基因。为此，我们猜测:UVB照射后，SLE发生异常自噬，miR-125b参与异常自噬的整个过程。针对此假设，本研究拟多层次观察UVB照射对SLE自噬的影响，以及miR-125b在异常自噬过程中的表达，通过选择性调控miR-125b表达技术及荧光素酶报告载体等方法验证miR-125b作用的下游自噬相关靶基因。研究结果有助于进一步阐明UVB、自噬和SLE三者之间的关系，并为研究紫外线诱发SLE的机制和防治提供新思路。

As one of the basic phenomeneons of cells, autophagy plays an important role in immunity system. It is well-known that ultraviolet B(UVB)can induce and aggravate SLE. Recent studies reveal that the level of autophagy in some skin cells can be affected by UVB. However,the effect of UVB on the autophagy of SLE is not still clarified. Our previous studies found that: The expression of miR-125b in peripheral blood mononuclear cells from patients with SLE and normal populations were significantly different after exposed to UVB. Meanwhile, miR-125b predicted downstream target sites of autophagy. Therefore, we propsoed the hypothesis: miR-125b may take part in the process of autophagy which meditates the pathogenesis of SLE. The present project intends to explore the impacts of UVB on the autophagy ability of SLE, and confirm miR-125b expression in the process. By selective regulation of miR-125b expression and dual-luciferase assay to confirm the downstream target genes of miR-125b. Our project will verify the effect of UVB on autophagy in SLE, and clarify the mechanism of miR-125b regulation of autophagy. Our project will also provide an experimeantal basis to learn about the possible mechanism of novel targets for the prevention and treatment of SLE.