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Original Article

^a Department of Dermatology, School of Medicine, Tokyo Medical and Dental University, Tokyo 113-8519, Japan
^b Department of Dermatology, School of Medicine, Nagasaki University, Nagasaki 852-8102, Japan
^c Department of Host Defense, Research Institute for Microbial Disease, Osaka University, Shuita, Osaka 565-0871, Japan
Department of Dermatology, School of Medicine, Tokyo Medical and Dental University, Yushi-ma-1-chome, 5-45, Bunkyo-ku, Tokyo 113-8519, Japan.81-3-5803-014381-3-5803-5286

3064.derm{at}med.tmd.ac.jp

Contact hypersensitivity (CHS) is thought to be mainly associated with the activation of T helper type 1 (Th1) cells. However, there is also evidence that Th2 cells or Th2 cytokines play a role in the development of CHS. To analyze the functional contribution of Th2 cytokines interleukin (IL)-4 and IL-13, signal transducer and activator of transcription 6 (STAT6)-deficient (STAT6^–/–) and wild-type (wt) control C57BL/6 mice were contact sensitized with 5% 2,4,6-trinitrochlorobenzene (TNCB), 0.5% 2,4-dinitrofluorobenzene, or 5% 4-ethoxyl methylene-2-phenyl-2-oxazolin-5-one, and any skin reactions were examined. Ear swelling was significantly reduced with a delayed peak response in STAT6^–/– mice compared with wt mice.

A histological analysis revealed that the infiltration of both eosinophils and neutrophils in the skin challenged after 24 h in STAT6^–/– mice decreased substantially compared with that in wt mice. The expression of Th2 cytokines (IL-4, IL-5) in TNCB-challenged skin tissues and the supernatants from T cells stimulated by 2,4,6-trinitrobenzene sulfonate–modified spleen cells, as well as the immunoglobulin (Ig)E and IgG1 response after challenge, were also profoundly reduced in STAT6^–/– mice, whereas the expression of interferon was the same in STAT6^–/– and wt mice after challenge. Furthermore, adoptive transfer experiments revealed that STAT6^–/– mice induced CHS after injection of lymph node cells obtained from sensitized wt mice. Our data suggest that the STAT6 signal plays a critical role in the induction phase of CHS.

Key Words: signal transducer and activator of transcription factor 6 • contact hypersensitivity • Th2 • IL-4 • IL-13

© 2000 The Rockefeller University Press

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