Interleukin-21 receptor signalling is not critically required for imiquimod-induced psoriasiform dermatitis in mice

Hee Joo Kim, Sung Hee Kim, Tae Gyun Kim, Je Yun Park, Minseok Lee, Dae Suk Kim, Min Geol Lee

Research output: Contribution to journalArticlepeer-review

2 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)191-195
Number of pages5
JournalExperimental dermatology
Volume27
Issue number2
DOIs
Publication statusPublished - 2018 Feb

Bibliographical note

Funding Information:
This work was supported by a grant from the Korea Health Technology R&D Project, Ministry of Health & Welfare, Republic of Korea (A121795 to Min-Geol Lee).

Publisher Copyright:
© 2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Molecular Biology
  • Dermatology

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