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Investigative Report

Antipruritic Effects of Janus Kinase Inhibitor Tofacitinib in a Mouse Model of Psoriasis

Takashi Hashimoto, Kent Sakai, Kristen M. Sanders, Gil Yosipovitch, Tasuku Akiyama
DOI: 10.2340/00015555-3086

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This article has been accepted for publication in Acta Dermato-Venereologica and is currently being edited and typeset. Readers should note that article shown below have been fully refereed, but have not been through the copy-editing and proof correction process. Only Abstract is possible to read. When this process is finalized the complete paper will be able to find.


The Janus kinase 1/3 inhibitor tofacitinib has demonstrated an antipruritic effect in two phase ΙΙΙ studies in psoriasis. However, the mechanisms behind this antipruritic effect are still unknown. We presently investigated whether tofacitinib affects spontaneous itch as well as expression of itch-related cytokines and epidermal nerve fiber density (ENFD) in the imiquimod-induced mouse model of psoriasis. Psoriasis-like skin lesions were produced by daily topical application of imiquimod to the back skin. Imiquimod treatment resulted in spontaneous scratching, which was significantly inhibited by tofacitinib treatment. Imiquimod treatment significantly increased mRNA expression of Il22, Il23, and Il31, reduced peptidergic ENFD, and increased nonpeptidergic ENFD compared to naive mice. Tofacitinib significantly decreased the expression of those cytokines and increased peptidergic ENFD without a significant effect on nonpeptidergic ENFD. Tofacitinib may inhibit psoriatic itch through inhibition of cytokine expression as well as modulation of epidermal innervation.

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