研究证实VD缺乏与SLE易感性密切相关，但其机制尚不完全明确。SLE中大量自体DNA免疫复合物(IC)通过NFκB信号持续激活DC是SLE免疫失衡的中心环节。VD可抑制NFκB家族中决定DC活化的关键分子RelB的表达而诱导DC耐受，但其可否通过抑制RelB的表达从而阻断DNA-IC刺激的DC活化尚不明确。本研究拟使用VD及自体DNA-IC刺激外周血DC，并将之皮下注射体外皮肤移植系统,观察DC成熟与活化表型、RelB基因表达及启动子VDRE区组蛋白乙酰化水平，并使用HDAC3基因沉默判断染色质重塑对VD调节DC免疫活性的影响。此后进一步将上述处理的DC与T细胞共培养，观察VD调控自体DNA-IC负载的DC对 SLE Treg/Th17免疫平衡的影响及其分子机制，最后使用狼疮鼠模型在体验证VD的调节作用，为今后探索使用VD协同自体DNA-IC诱导SLE免疫耐受奠定理论基础。

It has been confirmed that Vitamin D deficiency was associated with susceptibility to systemic lupus erythematosus(SLE), but its mechanisms are still unclear. Dendritic cells in SLE patients are continously stimulated by plenty of autoantibody-DNA immune complexes(IC)through NFκB signal,which is the key point in SLE immune imbalance.Vitamin D can induce DC tolerance by inihibiting the gene expression of NFκB family member RelB which is a critical regulator in DC maturation and differentiation.But it is unknown whether Vitamin D could inhibit DNA-IC stimulated DC activation by blocking RelB gene expression. In this study, DNA-IC and Vitamin D are used to stimulate peripheral blood DCs and are subcutaneously injected into Skin Explant System. The maturation of DC, RelB gene expression and the acetylation level of RelB gene VDRE area are detected. At the mean time, HDAC3 gene silence is used to observe the effects of chromatin remodeling on VitD regulated DC activity. Further, the DCs pretreated by DNA-IC and VitD are cocultured with T lymphocytes in order to observe the influences and mechanisms of VitD modulating DNA-IC stimulated DC activation on SLE Treg/Th17 immune balance. Finally, the lupus mouse model is used to verify the immune regulation effects of VitD in vivo. This study is proposed to establish the theoretical basis of VitD and auto DNA-IC induced SLE immune tolerance.