Previous studies have indicated that the autoimmune phenomenon might be caused by an imbalance of T helper cell (Th) cytokines. We measured the plasma concentrations of three novel proinflammatory cytokines interleukin (IL)-17, IL-18, IL-12 and a key Th2 cytokine IL-4 in patients with systemic lupus erythematosus (SLE) and correlated the ratio of proinflammatory/Th2 cytokines with SLE disease activity index (SLEDAI). Plasma IL-12, IL-17, IL-18 and IL-4 concentrations of 36 SLE patients and 18 sex- and age-matched control subjects were measured by enzyme linked immunosorbent assay. All were significantly higher in SLE patients than control subjects (IL-12, mean+/-s.d. of 166.7+/-84.5 vs 93.5+/-39.2 pg/ml, P<0.001; IL-17, 76.5+/-45.7 vs 37.6+/-35.3 pg/ml, P=0.002; IL-18, 368.7+/-199. 5 vs 141.1+/-47.1 pg/ml, P<0.001; and IL-4, 27.1+/-15.3 vs 17.3+/-7. 2 pg/ml, P<0.05), and IL-18/IL-4 ratio correlated positively and significantly with SLEDAI score (r=0.435, P=0.006). We propose that SLE is characterized by an elevation of both Th1 and Th2 cytokines: the elevation of proinflammatory cytokine IL-12, IL-17 and IL-18 may trigger the inflammatory process in SLE and the elevation of IL-18/IL-4 ratio suggests an imbalance of cytokine profile to mediate the inflammatory response.

SUMMARYAllergen-reactive T helper type-2 (Th2) cells and proinflammatory cytokines have been suggested to play an important role in the induction and maintenance of the inflammatory cascade in allergic asthma. We compared the plasma concentrations of novel proinflammatory cytokines IL-17 and IL-18, other proinflammatory cytokines IL-6 and IL-12, Th2 cytokines IL-10 and IL-13, and intracellular interferong (IFN-g) and IL-4 in Th cells of 41 allergic asthmatics and 30 sex-and age-matched health control subjects. Plasma cytokines were measured by enzyme-linked immunosorbent assay. Intracellular cytokines were quantified by flow cytometry. Plasma IL-18, IL-12, IL-10, IL-13 concentrations were significantly higher in allergic asthmatic patients than normal control subjects (IL-18: median 228´35 versus 138´72 pg/ml, P , 0´001; IL-12: 0´00 versus 0´00 pg/ml, P 0´001; IL-10: 2´51 versus 0´05 pg/ml, P , 0´034; IL-13: 119´38 versus 17´89 pg/ml, P , 0´001). Allergic asthmatic patients showed higher plasma IL-17 and IL-6 concentrations than normal controls (22´40 versus 11´86 pg/ml and 3´42 versus 0´61 pg/ml, respectively), although the differences were not statistically significant (P 0´077 and 0´053, respectively). The percentage of IFN-g-producing Th cells was significantly higher in normal control subjects than asthmatic patients (23´46 versus 5´72%, P , 0´001) but the percentage of IL-4 producing Th cells did not differ (0´72 versus 0´79%, P . 0´05). Consequently, the Th1/Th2 cell ratio was significantly higher in normal subjects than asthmatic patients (29´6 versus 8´38%, P , 0´001). We propose that allergic asthma is characterized by an elevation of both proinflammatory and Th2 cytokines. The significantly lower ratio of Th1/Th2 cells confirms a predominance of Th2 cells response in allergic asthma.

Among community-based middle-aged Chinese subjects, the metabolic syndrome was independent predictor of OSA.