PT  - JOURNAL ARTICLE
AU  - ANDREA BECKER-MEROK
AU  - GRO ØSTLI EILERTSEN
AU  - JOHANNES C. NOSSENT
TI  - Levels of Transforming Growth Factor-β Are Low in Systemic Lupus Erythematosus Patients with Active Disease
AID  - 10.3899/jrheum.100180
DP  - 2010 Oct 01
TA  - The Journal of Rheumatology
PG  - 2039--2045
VI  - 37
IP  - 10
4099  - http://www.jrheum.org/content/37/10/2039.short
4100  - http://www.jrheum.org/content/37/10/2039.full
SO  - J Rheumatol2010 Oct 01; 37
AB  - Objective. Cytokines are central regulators of the immune response but the workings of this complex network in systemic lupus erythematosus (SLE) are not fully understood. We investigated a range of inflammatory and immune-modulating cytokines to determine their value as biomarkers for disease subsets in SLE. Methods. This was a cross-sectional study in 102 patients with SLE (87% women, disease duration 10.6 yrs). Circulating concentrations of interleukin 1β (IL-1β), IL-4, IL-6, IL-10, IL-12, IL-17, monocyte chemotactic protein 1 (MCP-1), macrophage inflammatory protein 1 (MIP-1α), MIP-1β, interferon-γ (IFN-γ), tumor necrosis factor-α (TNF-α), and total transforming growth factor-β1 (TGF-β1) were related to disease activity (SLE Disease Activity Index; SLEDAI), lymphocyte subsets, autoantibody levels, accrued damage (Systemic Lupus International Collaborating Clinics/ACR Damage Index; SDI), and concomitant treatment. Results. Patients with SLE had lower levels of TGF-β1 (p = 0.01) and IL-1β (p = 0.0004) compared to controls. TGF-β1 levels were lower in patients with SLEDAI scores 1–10 and SDI > 3; and were correlated with CD4+, CD8+, and natural killer cell counts; and were independent of steroid or cytotoxic drug use. Treatment with cardiovascular drugs was associated with lower IL-12 levels. No consistent disease associations existed for the other cytokines investigated. Conclusion. Lower TGF-β1 was the most consistent cytokine abnormality in patients with SLE. The associations with disease activity, lymphocyte subsets, and damage suggest that TGF-β1 may be a therapeutic target of interest in SLE.