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JAK inhibitor JTE-052 regulates contact hypersensitivity by downmodulating T cell activation and differentiation.pdf
Journal of Dermatological Science 84 (2016) 258–265
Contents lists available at ScienceDirect
Journal of Dermatological Science
journal homepage:
JAK inhibitor JTE-052 regulates contact hypersensitivity by downmodulating T cell activation and differentiation
Wataru Amanoa,b, Saeko Nakajimaa, Yasuo Yamamotoa,b, Atsuo Tanimotob, Mutsuyoshi Matsushitab, Yoshiki Miyachia, Kenji Kabashima, MD PhDa,*
a Department of Dermatology, Kyoto University Graduate School of Medicine, Kyoto, Japan b Central Pharmaceutical Research Institute, Japan Tobacco, Japan
ARTICLE INFO
Article history: Received 11 April 2016 Received in revised form 8 September 2016 Accepted 13 September 2016
Keywords: JAK-STAT Contact hypersensitivity Skin in?ammation Cytokines Effector memory T cell
ABSTRACT
Background: Using JAK inhibitors to inhibit cytokine signaling is presumed to be a possible means of treating skin in?ammatory disorders such as contact dermatitis. Objective: To clarify the action site of JAK inhibitors in skin in?ammatory disorders. Methods: We analyzed the mechanism of action of the JAK inhibitor JTE-052 using murine skin in?ammation models, including contact hypersensitivity (CHS) and irritant contact dermatitis. Cells isolated from ear tissue or lymph node (LN) were analyzed by ?ow cytometry. The amounts of cytokines in the culture medium were measured by ELISA or bead array system. Proliferation of LN cells was evaluated by measurement of tritiated thymidine incorporation. Results: Oral administration of JTE-052 during both sensitization and elicitation phase attenuated CHS, but did not affect croton oil-induced irritant contact dermatitis. JTE-052 potently inhibited T cell proliferation and activation by antigen presentation in vitro, and attenuated skin in?ammation in a sensitized-lymphocyte transfer model without suppressing T cell migration. JTE-052 did not affect hapten-induced cutaneous dendritic cell migration into draining lymph nodes or their costimulatory molecule expres
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