Interleukin 17 (IL17)-producing T helper (Th17) cells, a new effector T cell subset, appear to play an essential role in autoimmune diseases.1 It has been shown that IL22 is another Th17 cytokine in mice and IL23 is critical for Th17 development.2^–5 Increased plasma IL17 levels have been reported in systemic lupus erythematosus (SLE).6 We analysed Th17-related cytokine profiles in the plasma of patients with SLE.

A total of 45 patients with SLE were studied. All patients received glucocorticoids (2.5–50 mg/day). There were 24 patients with active (SLE Disease Activity Index (SLEDAI) score of ⩾6; 22 female; mean (SD) age 37.3 (12.1)) and 21 with inactive disease (20 female; mean age 37.6 (11.8)). A total of 32 healthy subjects (30 female; mean age 38.3 (14.3)) were used as controls. Plasma samples were obtained under local ethics committee approved protocols and with informed consent. IL17, IL22 and IL23 levels were measured by sandwich enzyme-linked immunosorbent assay (all R&D Systems, Minneapolis, Minnesota, USA). Statistical analyses were performed using the Mann–Whitney U test and Spearman rank correlation test.

Plasma IL17 levels were significantly higher in active and inactive SLE (median (range): 79.0 (25.4–454.6) and 77.8 (27.5–487.6) pg/ml, respectively) than in controls (36.4 (15.7–338.2) pg/ml, p<0.001 and p<0.01, respectively), while no difference was found between patient groups (fig 1). Plasma IL22 levels were significantly decreased in active and inactive SLE (28.2 (<15.6–104.2) and 162.3 (26.1–559.7) pg/ml, respectively) compared with controls (378.8 (21.8–1154.2) pg/ml, p<0.001 and p<0.05, respectively), although higher in inactive SLE compared with active SLE (p<0.001). Plasma IL23 levels were shown pronounced increase in active and inactive SLE (13.8 (<7.8–247.5) and 20.8 (<7.8–234.6) pg/ml, respectively) compared with controls (<7.8 (<7.8–81.7) pg/ml, p<0.01 and p<0.001, respectively), with no difference between patient groups.

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Figure 1

Plasma levels of interleukin (IL)17, IL22 and IL23 in healthy controls (n = 32), and active systemic lupus erythematosus (SLE) (n = 24) and inactive SLE (n = 21). Horizontal bars indicate the median.

A strong correlation was found between IL17 and IL23 levels (r_s = 0.753; p<0.001) in all patients with SLE. IL22 levels in all patients correlated significantly with SLEDAI, erythrocyte sedimentation rate (ESR), anti-dsDNA antibody and complement 3 (C3) (table 1). Three cytokine levels were not associated with specific manifestations and glucocorticoid treatment.

IL17 can induce the expression of multiple inflammatory mediators and its receptor is ubiquitously distributed in various tissues.1 IL23 can promote the generation of human Th17 cells expressing IL17 and IL22.4 5 Thus, our findings of increased IL17 and IL23 levels in SLE, with a good correlation between two levels, could indicate Th17-mediated inflammation in SLE. However, we observed low IL22 levels relevant to disease activity in SLE. Emerging data indicate proinflammatory and anti-inflammatory properties of IL22 in inflammatory response.3 7^–9 Furthermore, a recent paper reported the presence of specific IL22-producing CD4⁺ T cell subset distinct from Th17 and Th1 cells in human peripheral blood.10 The source and biological activities of IL22 may, therefore, substantially differ from that of IL17.

In conclusion, increased plasma IL17 and IL23 and decreased IL22 in SLE may suggest their important and distinct roles in SLE pathophysiology, though it is impossible to determine causal relationships in this cross-sectional study.