Levels of IL36 alpha are known to be increased in specimens from patients with atopic dermatitis and psoriasis. In addition, it has been reported that IL-36 alpha is crucial for development of imiquimod-induced psoriatic dermatitis in mice. On the other hand, the role of IL-36 alpha in induction of allergic contact dermatitis/contact hypersensitivity (ACD/CHS) is poorly understood. We found that IL-36 alpha was produced in keratinocytes of mice during imiquimod-induced psoriatic dermatitis, but it was hardly detectable in the skin of mice during either fluorescein isothiocyanate (FITC)- or 1-fluoro-2, 4-dinitrobenzene (DNFB)-induced CHS. Although IL-36 alpha can enhance activation of dendritic cells (DCs) and T cells, in CHS, IL-36a was not essential for DC migration from the skin to draining LNs, but it was required for induction or activation of hapten-specific T cells such as Th/Tcl or Th17 cells. However, local inflammation, assessed by measurement of ear skin thickness, was comparable between wild-type and IL-36 alpha-deficient mice during both FITC- and DNFB-induced CHS. These observations indicate that IL-36 alpha is involved in induction and/or activation of hapten-specific T-cell subsets in the sensitization phase of CHS, but not essential for induction of local inflammation in the elicitation phase. (C) 2018 Elsevier Inc. All rights reserved.