Open AccessRIG‐I antiviral signaling drives interleukin‐23 production and psoriasis‐like skin disease
Author(s) -
Zhu Huiyuan,
Lou Fangzhou,
Yin Qianqian,
Gao Yuanyuan,
Sun Yang,
Bai Jing,
Xu Zhenyao,
Liu Zhaoyuan,
Cai Wei,
Ke Fang,
Zhang Lingyun,
Zhou Hong,
Wang Hong,
Wang Gang,
Chen Xiang,
Zhang Hongxin,
Wang Zhugang,
Ginhoux Florent,
Lu Chuanjian,
Su Bing,
Wang Honglin
Publication year - 2017
Publication title -
embo molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.923
H-Index - 107
eISSN - 1757-4684
pISSN - 1757-4676
DOI - 10.15252/emmm.201607027
Subject(s) - psoriasis , immunology , disease , interleukin , medicine , interleukin 23 , cytokine , pathology
Retinoic acid inducible‐gene I ( RIG ‐I) functions as one of the major sensors of RNA viruses. DDX 58 , 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‐ds RNA , 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 CD 11c + dendritic cells ( DC s) via nuclear factor‐kappa B ( NF ‐κB) signaling, and stimulated RIG ‐I expression in an auto‐regulatory feedback loop. Thus, our data suggest that the dysregulation in the antiviral immune responses of hosts through the innate pattern recognition receptors may trigger the skin inflammatory conditions in the pathophysiology of psoriasis.