Abstract: Objective To investigate the relationship between vitamin D and endothelial progenitor cells in patients with active systemic lupus erythematosus （SLE）, and to reveal the intrinsic causes of atherosclerosis in SLE. Methods Thirty consecutive patients （SLEDAI score≥8） were in the active phase of SLE who attended the in-patient clinic of our hospital and 30 age and sex-matched healthy people as controls. Ezyme linked immune sorbent assay（ELISA） was used to detect the levels of 25-Dihydroxyvitamin D25（OH）Din peripheral blood. Isolation and culture of endothelial progenitor cells（EPC）by density gradient centrifugation and adherent culture. CD3⁺/CD4⁺/VEGFR-2⁺EPC numbers were determined by flow cytometry. Migration and adhesion of EPCs were observed by transwell migration assay. Statistical analysis was conducted with t-test and Mann-Whitney rank test. Results ① The level of peripheral blood 25（OH）D in patients with active SLE （14.47±10.39） ng/mL was lower than normal controls（24.15±7.98） ng/mL （P<0.05）. ②In active SLE subgroups, the number of EPC（0.028%±0.017%） were significantly lower than normal controls （0.067%±0.012%） （P<0.05）. The migration rate of EPC from active SLE patients（1.7‰±0.9‰） were significantly reduced as compared with normal controls（3.1‰±1.6‰） （P<0.05）. The adhesion of EPCs from active SLE patients（19±7）were declined as compared with normal controls（34±11）（P<0.05）. ③The level of peripheral blood 25（OH）D was positively correlated with the number of EPC in active SLE（P<0.05）. The level of peripheral blood 25（OH）D was positively correlated with the migration and adhesion of EPC in active SLE（P<0.05）. Conclusion The study demonstrate an association between EPC reduction/dysfunction and vitamin D insufficiency in SLE patients, which results in endothelial dysfunction and atherosclerosis. These findings can provide strong rationale for atherosclerosis therapy in SLE.