IL-23 induces regulatory T cell plasticity with implications for inflammatory skin diseases.

ABSTRACT: Foxp3⁺ regulatory T cells (Tregs) represent a major fraction of skin resident T cells. Although normally protective, Tregs have been shown to produce pro-inflammatory cytokines in human diseases, including psoriasis. A significant hurdle in the Treg field has been the identification, or development, of model systems to study this Treg plasticity. To overcome this gap, we analyzed skin resident Tregs in a mouse model of IL-23 mediated psoriasiform dermatitis. Our results demonstrate that IL-23 drove the accumulation of Tregs; including a subpopulation that co-expressed RORγt and produced IL-17A. Genesis of this population was attenuated by a RORγt inverse agonist compound and clinically relevant therapeutics. In vitro, IL-23 drove the generation of CD4⁺Foxp3⁺

SUBMITTER: Kannan AK 

PROVIDER: S-EPMC6881359 | biostudies-literature | 2019 Nov

REPOSITORIES: biostudies-literature