IL-36α is involved in hapten-specific T-cell induction, but not local inflammation, during contact hypersensitivity
| Autor: | Susumu Nakae, Yoichiro Iwakura, Takafumi Numata, Kazutoshi Harada, Takamichi Yoshizaki, Katsuko Sudo, Ryoji Tsuboi, Sachiko Yamaguchi, Eri Shimura |
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| Rok vydání: | 2018 |
| Předmět: |
Keratinocytes
0301 basic medicine T-Lymphocytes T cell Biophysics Dermatitis Inflammation Dermatitis Contact Biochemistry 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Cell Movement Psoriasis medicine Animals Fluorescein isothiocyanate Molecular Biology Allergic contact dermatitis Sensitization Skin Imiquimod integumentary system Dendritic Cells Cell Biology Atopic dermatitis medicine.disease Mice Inbred C57BL 030104 developmental biology medicine.anatomical_structure chemistry Immunology Lymph Nodes medicine.symptom Haptens Hapten Interleukin-1 030215 immunology |
| Zdroj: | Biochemical and Biophysical Research Communications. 506:429-436 |
| ISSN: | 0006-291X |
| Popis: | Levels of IL36α are known to be increased in specimens from patients with atopic dermatitis and psoriasis. In addition, it has been reported that IL-36α is crucial for development of imiquimod-induced psoriatic dermatitis in mice. On the other hand, the role of IL-36α in induction of allergic contact dermatitis/contact hypersensitivity (ACD/CHS) is poorly understood. We found that IL-36α 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-36α can enhance activation of dendritic cells (DCs) and T cells, in CHS, IL-36α 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 Th17 cells. However, local inflammation, assessed by measurement of ear skin thickness, was comparable between wild-type and IL-36α-deficient mice during both FITC- and DNFB-induced CHS. These observations indicate that IL-36α 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. |
| Databáze: | OpenAIRE |
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