EDITORIAL - TGF-beta level: indicator for severity of disease and organ damage in SLE

[Guest guest]

Journal of Rheumatology

Editorial

Oct 2010

Transforming Growth Factor-β Level: Indicator for Severity of Disease

and Organ Damage in Patients with Systemic Lupus Erythematosus

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.

http://jrheum.org/content/37/10/1983.full

Not an MD