| First Author | Numata T | Year | 2018 |
| Journal | Biochem Biophys Res Commun | Volume | 506 |
| Issue | 3 | Pages | 429-436 |
| PubMed ID | 30352688 | Mgi Jnum | J:268851 |
| Mgi Id | MGI:6272496 | Doi | 10.1016/j.bbrc.2018.10.104 |
| Citation | Numata T, et al. (2018) IL-36alpha is involved in hapten-specific T-cell induction, but not local inflammation, during contact hypersensitivity. Biochem Biophys Res Commun 506(3):429-436 |
| abstractText | Levels of IL36alpha are known to be increased in specimens from patients with atopic dermatitis and psoriasis. In addition, it has been reported that IL-36alpha is crucial for development of imiquimod-induced psoriatic dermatitis in mice. On the other hand, the role of IL-36alpha in induction of allergic contact dermatitis/contact hypersensitivity (ACD/CHS) is poorly understood. We found that IL-36alpha 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-36alpha can enhance activation of dendritic cells (DCs) and T cells, in CHS, IL-36alpha 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/Tc1 or Th17cells. However, local inflammation, assessed by measurement of ear skin thickness, was comparable between wild-type and IL-36alpha-deficient mice during both FITC- and DNFB-induced CHS. These observations indicate that IL-36alpha 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. |
