Elevation of proinflammatory cytokine (IL-18, IL-17, IL-12) and Th2 cytokine (IL-4) concentrations in patients with systemic lupus erythematosus
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...
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Published in | Lupus Vol. 9; no. 8; pp. 589 - 593 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
Thousand Oaks, CA
SAGE Publications
01.01.2000
Sage Publications Ltd |
Subjects | |
Online Access | Get full text |
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Summary: | 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 proin/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. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2 |
ISSN: | 0961-2033 1477-0962 |
DOI: | 10.1191/096120300678828703 |