Abstract:
BACKGROUND:Using JAK inhibitors to inhibit cytokine signaling is presumed to be a possible means of treating skin inflammatory disorders such as contact dermatitis. OBJECTIVE:To clarify the action site of JAK inhibitors in skin inflammatory disorders. METHODS:We analyzed the mechanism of action of the JAK inhibitor JTE-052 using murine skin inflammation models, including contact hypersensitivity (CHS) and irritant contact dermatitis. Cells isolated from ear tissue or lymph node (LN) were analyzed by flow 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 inflammation 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 expressions. CONCLUSION:The JAK inhibitor JTE-052 exerts an inhibitory effect on antigen-specific T cell activation and subsequent inflammation in acquired skin immunity, such as CHS.
journal_name
J Dermatol Scijournal_title
Journal of dermatological scienceauthors
Amano W,Nakajima S,Yamamoto Y,Tanimoto A,Matsushita M,Miyachi Y,Kabashima Kdoi
10.1016/j.jdermsci.2016.09.007subject
Has Abstractpub_date
2016-12-01 00:00:00pages
258-265issue
3eissn
0923-1811issn
1873-569Xpii
S0923-1811(16)30769-1journal_volume
84pub_type
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