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Interleukin‐21 receptor signalling is not critically required for imiquimod‐induced psoriasiform dermatitis in mice
Author(s) -
Kim Hee Joo,
Kim Sung Hee,
Kim TaeGyun,
Park Je Yun,
Lee Minseok,
Kim Dae Suk,
Lee MinGeol
Publication year - 2018
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/exd.13481
Subject(s) - psoriasis , imiquimod , immunology , cytokine , inflammation , interleukin 17 , interleukin 23 , medicine , interleukin 10 , interleukin
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 CD 4+ 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.