The present study aimed to investigate the levels of IL-36α and its association with disease activity in patients with systemic lupus erythematosus (SLE). A total of 60 patients with SLE and 29 healthy controls were enrolled in the present study. Disease activity was evaluated using the SLE disease activity index (SLEDAI). The serum levels of IL-36α, IL-36 receptor antagonist (IL-36Ra) and IL-17 were assessed using ELISA. The levels of IL-36α in patients with SLE were significantly higher

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... ed with those of healthy controls. There was a significant increase in IL-36α in the active SLE group (SLEDAI score ≥5) compared with that of the healthy controls (P<0.001). The serum IL-36α levels were higher in patients with active SLE than in patients with quiescent disease (P=0.012). IL-36Ra was downregulated in patients with SLE (P=0.007). The serum IL-17 levels were elevated in patients with SLE (P=0.036), and a positive correlation was observed between the IL-36α and IL-17 levels (r=0.453, P=0.003). The serum IL-36α levels were associated with SLEDAI (r=0.374, P=0.003), proteinuria (r=0.329, P=0.010) and complement 3 (r=-0.336, P=0.009). Patients who were receiving glucocorticoid treatment had lower IL-36α levels than those who were not receiving glucocorticoid treatment (P=0.003). Patients with lupus nephritis had higher serum IL-36α levels compared with those found in patients without lupus nephritis (P=0.037). The serum IL-36α concentration was elevated in patients with SLE, and was correlated with disease activity and IL-17 levels. The aberrant serum IL-36α levels observed in the present study and its clinical association with SLE suggest the important role of IL-36α in onset and progression of SLE. In addition, the association of IL-36α with IL-17 level indicates its involvement in the regulation of T helper 17 cytokines.