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Etanercept decreases the innate immune wounding response in psoriasis
Author(s) -
Hata Tissa R.,
Afshar Maryam,
Miller Jeremiah,
Two Aimee M.,
Kotol Paul,
Jackson Michelle,
Alexandrescu Doru T.,
Kabigting Filamer,
Gerber Monika,
Lai Yuping,
Gallo Richard L.
Publication year - 2013
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/exd.12167
Subject(s) - etanercept , psoriasis , innate immune system , immunology , immune system , medicine , tumor necrosis factor alpha
Abstract Cathelicidin is increased when normal skin is injured and in psoriasis lesions where it has been suggested to play a pivotal role in inflammation through interactions with self‐ DNA and toll‐like receptor 9 ( TLR ‐9) in keratinocytes and plasmacytoid dendritic cells. Because of etanercept's success in treating psoriasis, we hypothesized that etanercept may suppress TLR ‐9 and cathelicidin induction. Examination of experimentally induced wounds of psoriatic lesional and non‐lesional skin, and comparison with wounded normal skin, shows that the induction of cathelicidin and TLR ‐9 is greatly enhanced in lesional psoriatic skin. Six weeks of etanercept appears not to affect the baseline expression of cathelicidin or TLR ‐9, but does blunt the induction of cathelicidin in psoriasis with wounding. These findings support the role of cathelicidin in the enhancement of local inflammation in psoriasis and may partially explain one of the mechanisms enabling TNF ‐α inhibitors to successfully treat this disorder.