Will a Biologic Agent Be Useful for Managing Lupus-Associated Skin Disease?

A targeted tumor-necrosis-factor–receptor biologic agent improved skin lesions in mice.

The pathogenesis of skin disease in patients with lupus erythematosus (LE) is still being unraveled. Inflammatory mediators appear to be involved, and blocking their activity might prevent LE-related skin disease. For example, tumor necrosis factor α (TNF-α) binds to the extracellular domains of two TNF receptors — TNFRI (p60) and TNFRII (p80). The TNF-receptor preligand assembly domain (PLAD), which mediates the receptor-chain association essential for signaling, has been shown to block the effects of TNF-α and to inhibit the inflammatory arthritis that it induces. A recent study demonstrates that the use of p60 could inhibit the development of skin lesions in a mouse model of systemic LE.

These researchers administered p60, p80, or placebo…

Reviewing Author

Jeffrey P. Callen, MD

Disclosures

Consultant / Advisory board XOMA; Eli Lilly; Celgene

Equity Various trust accounts

Editorial boards JAMA Dermatology; UpToDate

Leadership positions in professional societies Association of Professors of Dermatology (President-Elect)