Expression profiles of whole skin samples from keratinocyte-specific TRAF6 deficient mice treated with and without IMQ treatment

Tumor necrosis factor receptor associated factor 6 (TRAF6) is an adaptor protein that regulates NF-B and MAPK signaling pathway and is reported to affect immune response and cell death in immune cells. However, the roles of TRAF6 in epithelium have not been well investigated. Using a mouse model of imiquimod-induced psoriasis dermatitis, we show that TRAF6 in epithelial cells totally regulates IL-17-mediated inflammation in the skin. Mice lacking TRAF6 in keratinocytes were unable to activate dendritic cells and failed to produce IL-23 or initiate IL-17 production from T cells at the imiquimod-treated sites. Subcutaneous administrations of IL-23 restored IL-17 production in the mutant animals, suggesting that the induction of IL-23 production is the major TRAF6-dependent contribution of keratinocytes to this process. Therefore, the epithelial TRAF6 signaling is supposed to play an essential role in instructing and propagating the cutaneous immune response.

4

Matsumoto R, Dainichi T, Tsuchiya S, Nomura T, Kitoh A, Hayden MS, Ishii KJ, Tanaka M, Honda T, Egawa G, Otsuka A, Nakajima S, Sakurai K, Nakano Y, Kobayashi T, Sugimoto Y, Kabashima K