Cutting edge: PD-1 regulates imiquimod-induced psoriasiform dermatitis through inhibition of IL-17A expression by innate γδ-low T cells

Yasutomo Imai, Natarajan Ayithan, Xuesong Wu, Ying Yuan, Li Wang, Samuel T Hwang

Research output: Contribution to journalArticle

24 Scopus citations

Abstract

Programmed cell death 1 (PD-1) is a key regulatory molecule that has been targeted in human cancers, including melanoma. In clinical testing, Abs against PD-1 have resulted in psoriasiform dermatitis (PsD). To determine whether PD-1 regulates PsD, we compared skin responses of PD-1-deficient (PD-1KO) mice and wild-type (WT) controls in an imiquimod (IMQ)-induced murine model of psoriasis. PD-1KO mice showed severe epidermal hyperplasia, greater neutrophilic infiltration, and higher expression of Th17 cytokines (versus WT mice). IMQ exposure increased PD-1 expression by skin γδ-low (GDL) T cells and enhanced expression of PD-L1 by keratinocytes. Three-fold increases in the percentage of IL-17A+ GDL T cells were observed in skin cell suspensions derived from IMQ-treated PD-1KO mice (versus WT controls), suggesting that the lack of PD-1 has a functional effect not only on αβ T cells, but also on GDL T cells, and that PD-1 may play a regulatory role in PsD.

Original languageEnglish (US)
Pages (from-to)421-425
Number of pages5
JournalJournal of Immunology
Volume195
Issue number2
DOIs
StatePublished - Jul 15 2015
Externally publishedYes

ASJC Scopus subject areas

  • Immunology
  • Medicine(all)

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