RESEARCH ARTICLE Effects of tofacitinib on ly d r

NYO 219/07/01, New York, NY 10017, USA Full list of author information is available at the end of the articlePsoriasis is a debilitating and recurring immune-mediated inflammatory disease that affects 0.91–8.5 % of the adult population according to geographic region [1]. Plaque psoriasis is by far the most prevalent form, accounting for approximately 80 % of cases [2]. Tofacitinib is an oral Janus kinase (JAK) inhibitor that is being investigated for psoria-sis. Oral tofacitinib has been evaluated in a Phase I study Phase III studies in patients with chronic plaque psoriasis [4-6] (see also NCT01276639 and NCT01309737). Tofaci-tinib binds to and inhibits JAK1 and JAK3, thereby block-ing pro-inflammatory cytokine signaling, in particular interleukin (IL)-6 and interferon γ [7,8]. C-reactive protein (CRP), a marker of inflammation, is under the transcrip-tional control of IL-6 [9] and, thus, may be modulated by tofacitinib. Tofacitinib also modulates the activity of sev-eral other interleukins (including IL-2, −4, −7, −9, −15, and −21) that have roles in mediating immune response to viral infection/reactivation, lymphocyte development, an