EDITORIAL - On anti-TNF-induced SLE

[Guest guest]

Journal of Rheumatology

Editorial

Jan 2010

On Anti-Tumor Necrosis Factor-induced Systemic Lupus Erythematosus

In the 1950s and 1960s Geritol tonic was heavily advertised on

television as a fast cure-all if “you’re feeling weak and rundown,

tired or nervous.†It was lampooned in a more recent sitcom as a magic

elixir capable of transforming a friendless geek into the most popular

kid at school. While the recent and numerous television advertisements

for the anti-tumor necrosis factor (TNF) agents currently on the

market do not make such outlandish claims as this, one cannot help but

be awed by the overwhelming presence that these intravenously infused

prescription drugs have so quickly established in the public sphere.

TNF-α generates a vast array of biological properties, including

cellular differentiation, proliferation, and apoptosis1–4. This

variability is attributed to the binding of TNF to 2 distinct

transmembrane receptors that can mediate TNF-induced inflammation and

cell death, the promotion of proliferative responses in T lymphocytes

and other hematopoietic cells5–7, and the induction of apoptosis in

mature activated T cells8. Thus, TNF can serve dually as a potent

proinflammatory mediator and a key immune modulator.

Due to the multifarious effects of TNF, the results of either TNF

administration or blockade have varied significantly from disease to

disease and from animal models to human patients. In terms of TNF

blockade, currently 3 anti-TNF agents are licensed for clinical use

(the 2 monoclonal antibodies adalimumab and infliximab and a soluble

TNF receptor, etanercept) and are prescribed for the treatment of

rheumatoid arthritis (RA), juvenile RA, psoriatic arthritis, chronic

inflammatory bowel disease (IBD), and ankylosing spondylitis9,10.

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Read the whole editorial here:

http://www.jrheum.org/content/37/1/3.full

Not an MD