Transforming Growth Factor-β Level: Indicator for Severity of Disease and Organ Damage in Patients with Systemic Lupus Erythematosus: Figure 1.

Abstract

Systemic lupus erythematosus (SLE) is a T cell-dependent disorder of generalized autoimmunity characterized by B cell hyperactivity with numerous autoantibodies. Studies in both experimental animal models of lupus and patients with SLE have revealed a number of cytokine pathways that are important in the disease process. An imbalance between pro- and antiinflammatory cytokines might be responsible for the pathogenesis and development of SLE. For example, serum levels of interferon-α (IFN-α), tumor necrosis factor-α (TNF-α), IFN-γ, interleukin 1 (IL-1), IL-6, IL-18, and B cell activating factor are increased in patients with SLE in comparison with healthy individuals and have been shown to correlate with disease activity. Anticytokine and anticytokine receptor therapy have shown a significant decrease in disease activity in SLE and other autoimmune diseases, further suggesting that enhanced proinflammatory cytokines are associated with disease development. Conversely, a decreased ability of T cells to produce immunosuppressive cytokines such as transforming growth factor-β (TGF-β) has been reported1. In contrast, IL-10 is another immunosuppressive cytokine whose level is actually elevated in active SLE. Although IL-10 can suppress T helper cell and dendritic cell responses, it has a strong stimulatory effect on B cells. This feature of IL-10 makes it deleterious in SLE development. Despite the previous study documenting a decreased ability of SLE T cells to produce TGF-β1, questions concerning the value of serum TGF-β in SLE pathogenesis and development remain unresolved. Many cells such as lymphocytes, monocytes, and natural killer (NK) cells can produce TGF-β and its biological half-life in serum is very short due to quick degradation to its inactive form. In fact, early studies revealed no significant differences of levels of bioactive TGF-β in serum between healthy control subjects and patients with inactive and active SLE2. However, in their study in this issue … Address correspondence to Dr. Zheng. E-mail: szheng{at}usc.edu