Objective:To observe the expression of interleukin (IL)-38 in patients with active systemic lupus erythematosus (SLE), and to explore the regulatory effect of IL-38 on IκB kinase complex.Methods:The gene expression levels of IL-38 and IκB kinase complex were detected by real-time fluorescence quantitative polymerase chain reaction (PCR). Serum IL-38 levels were detected by enzyme-linked immunosorbent assay (ELISA). The expression of IκB-kinase complex (IκK)α/β and phospho IκKα/β protein weredetermined by Western blotting analysis. Statistical analysis was conducted with or Mann-Whitney rank test.Results:① The expression level of IL-38 mRNA in active SLE patients (0.36±0.09) was significantly lower than that in the normal control group (1.00±0.17) ( Z=-4.07, P<0.01); the expression level of IL-38 protein in active SLE patients (5.86±2.76) significantly reduced as compared with normal control group (18.48±1.35) ( Z=-4.76, P<0.05). ② The expression level of IκKα mRNA (7.45±0.31) and IκKβ mRNA (6.01±1.51) in active SLE patients was significantly higher than that in normal control group (1.16±0.04) and (1.16±0.14) ( Z=-4.67, P<0.05; Z=-4.37, P<0.01), and the expression level of IL-38 mRNA was negatively correlated with IκKα mRNA and IκKβ mRNA in active SLE patients ( r=-0.78, P<0.05; r=-0.83, P<0.05). ③ IκKα/β and phosphorylated IκKα/β protein expression in active SLE patients (2.38±0.03) and (1.90±0.03) increased significantly compared with healthy controls (1.00±0.04) and (1.00±0.08) ( Z=-1.96, P<0.05; Z=-1.99, P<0.05). ④ In vitro experiment, IL-38 caused a significant decrease in the expression level of IκKα mRNA (1.70±0.12) and IκKβ mRNA (2.52±0.10) from active SLE patientscompared with untreated cells (2.56±0.28) and (3.82±0.38) ( Z=-1.96, P<0.05; Z=-1.37, P<0.05). ⑤ In vitro experiment, IL-38 caused a significant decrease in the expression level of IκKα/β (1.54±0.06) and phosphoryl-ated IκKα/β (0.970±0.012) protein expression in active SLE patients compared with untreated cells (2.93±0.08) and (1.572±0.051)( P<0.05). Conclusion:The de-crease of IL-38 level in SLE patients result in the excessive activation of IκB kinase complex IκKα and IκKβ, and therefore triggersystemic lupus erythematosus.