Interactions between TNF-like weak inducer of apoptosis and its receptor Fn14 are significantly associated with the pathogenesis of cutaneous lupus, according to Dr. Jessica Doerner and her associates.

Treating murine keratinocytes with TWEAK stimulated both RANTES, a T cell important in the pathogenesis of psoriasis and atopic dermatitis, and apoptosis, indicating the presence of the Fn14 receptor. Ultraviolet B radiation also increased Fn14 expression and RANTES production, with the effect further increased when both TWEAK and UVB light were present. In a small human sample, three out of three skin samples from lesional lupus patients showed significant Fn14 staining.

“We propose that the TWEAK/Fn14 axis contributes to the pathogenesis of cutaneous lupus, and that this signaling pathway represents a potential therapeutic target for biological agents,” the investigators concluded.

Find the full study in the Journal of Investigative Dermatology (doi: 10.1038/jid.2015.124).


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