RIG-I antiviral signaling drives interleukin-23 production and psoriasis-like skin disease.

ABSTRACT: Retinoic acid inducible-gene I (RIG-I) functions as one of the major sensors of RNA viruses. DDX58, which encodes the RIG-I protein, has been newly identified as a susceptibility gene in psoriasis. Here, we show that the activation of RIG-I by 5'ppp-dsRNA, its synthetic ligand, directly causes the production of IL-23 and triggers psoriasis-like skin disease in mice. Repeated injections of IL-23 to the ears failed to induce IL-23 production and a full psoriasis-like skin phenotype, in either germ-free or RIG-I-deficient mice. RIG-I is also critical for a full development of skin inflammation in imiquimod (IMQ)-induced psoriasis-like mouse model. Furthermore, RIG-I-mediated endogenous IL-23 production was mainly confined to the CD11c⁺ dendritic cells (DCs) via nuclear facto

SUBMITTER: Zhu H 

PROVIDER: S-EPMC5412807 | biostudies-literature | 2017 May

REPOSITORIES: biostudies-literature