Foxp3⁺ T reg cells control psoriasiform inflammation by restraining an IFN-I-driven CD8⁺ T cell response.

ABSTRACT: Psoriasis is a complex inflammatory skin disease affecting ∼3% of the population worldwide. Although type I interferons (IFN-I) are thought to be involved in its pathogenesis, the details of this relationship remain elusive. Here we show that in a murine model of imiquimod-driven psoriatic skin inflammation, Foxp3⁺ regulatory T cells (T reg cells) control inflammation severity by restraining IFN-I. Depletion of T reg cells induces IFN-I and IFN-stimulated gene expression, and leads to accumulation of CD8⁺ T cells in lesional skin. Mononuclear phagocytes (MNPs) were the source of IFN-I, and their depletion reversed the effect of T reg cell depletion. Blockade of IFN-I signaling abolished CD8⁺ T cell infiltration and excess inflammation in the skin of T reg c

SUBMITTER: Stockenhuber K 

PROVIDER: S-EPMC6080913 | biostudies-literature | 2018 Aug

REPOSITORIES: biostudies-literature