1. Interleukin-21 receptor signalling is not critically required for imiquimod-induced psoriasiform dermatitis in mice
- Author
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Dae Suk Kim, Hee Joo Kim, Tae-Gyun Kim, Je Yun Park, Sung Hee Kim, Minseok Lee, and Min Geol Lee
- Subjects
0301 basic medicine ,CD4-Positive T-Lymphocytes ,Interferon Inducers ,medicine.medical_treatment ,Inflammation ,Dermatitis ,Mice, Transgenic ,Dermatology ,Biochemistry ,Interleukin 22 ,03 medical and health sciences ,Mice ,0302 clinical medicine ,Psoriasis ,Interleukin 23 ,medicine ,Animals ,Molecular Biology ,Intraepithelial Lymphocytes ,Mice, Knockout ,Imiquimod ,business.industry ,Interleukin ,Interleukin-21 Receptor alpha Subunit ,medicine.disease ,030104 developmental biology ,Cytokine ,Interleukin-21 receptor ,Immunology ,Interleukin-23 Subunit p19 ,Receptors, Interleukin-21 ,Interleukin 17 ,medicine.symptom ,business ,030215 immunology ,Signal Transduction - Abstract
Psoriasis is largely mediated by interleukin (IL)-23/T helper (Th) 17 axis, and IL-21 is a pleiotropic cytokine expressed by Th17 cells. Despite previously reported possible pathogenic roles of IL-21 in human psoriasis, we found that IL-21 receptor (IL-21R) signalling was not crucial for imiquimod-induced psoriatic inflammation, using IL-21R−/− mice. The severity of imiquimod-induced psoriatic manifestation and pro-inflammatory Th17 cytokine levels, IL-17A-producing γδ T cells and CD4+ T cells, and in vitro IL-17A production by γδ T cells after IL-23 stimulation was comparable between wild-type and IL-21R−/− mice. Collectively, IL-21R signalling was not critically involved in IMQ-induced psoriatic inflammation despite an increased IL-21 expression in the IMQ-treated mouse skin. Our data may represent the significant differences between human psoriasis and murine psoriasis model, and further studies using other models will be required to elucidate the role of IL-21 in psoriasis pathogenesis.
- Published
- 2017