The contribution of IL-17 to the development of autoimmunity in psoriasis

Masutaka Furue, Takafumi Kadono

Research output: Contribution to journalReview articlepeer-review

10 Citations (Scopus)

Abstract

Psoriasis is an (auto)immune-mediated disease that manifests as widespread desquamative erythema. The TNF-α/IL-23/IL-17A axis is crucial to its pathogenesis, which is demonstrated by its excellent therapeutic response to biologics that target this axis. There is a strong association between HLA-C*0602 and psoriasis, and researchers have identified autoantigens that are restricted to this major histocompatibility class I molecule. These auto-Ags include LL-37, A disintegrin and metalloprotease domain containing thrombospondin type 1 motif-like 5 (ADAMTSL5), and keratin 17. IL-17A-producing T cells have been identified in T cell populations that are reactive to these auto-Ags. In addition, lipid Ags have surfaced as candidate auto-Ags that activate IL-17A-producing T cells in a CD1a-restricted manner. In this article, we review the candidate auto-Ags that may contribute to the activation of the IL-17A-deviated immune response in psoriasis.

Original languageEnglish
Pages (from-to)337-343
Number of pages7
JournalInnate Immunity
Volume25
Issue number6
DOIs
Publication statusPublished - Aug 1 2019

All Science Journal Classification (ASJC) codes

  • Microbiology
  • Immunology
  • Molecular Biology
  • Cell Biology
  • Infectious Diseases

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