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

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机构: [1]Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Department of Immunology and Microbiology, Shanghai Institute of Immunology, Shanghai Jiao Tong University School of Medicine (SJTU-SM), Shanghai, China [2]Department of Dermatology, Xijing Hospital, The Fourth Military Medical University, Xi’an, China [3]Department of Dermatology, Xiangya Hospital, Central South University, Changsha, China [4]Research Centre for Experimental Medicine of Rujin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China [5]Singapore Immunology Network (SIgN), Agency for Science, Technology and Research (A*STAR), Singapore City, Singapore [6]Guangdong Provincial Hospital of Chinese Medicine, Guangdong Provincial Academy of Chinese Medical Sciences, The Second Clinical School of Guangzhou University of Chinese Medicine, Guangzhou, China [7]Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Shanghai Jiao Tong University School of Medicine (SJTU-SM), Shanghai, China
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关键词: DCs interleukin-23 NF-kappa B psoriasis RIG-I

摘要:
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 factor-kappa B (NF-kappa B) 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.

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出版当年[2016]版:
大类 | 1 区 医学
小类 | 1 区 医学:研究与实验
最新[2025]版:
大类 | 1 区 医学
小类 | 1 区 医学:研究与实验
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出版当年[2015]版:
Q1 MEDICINE, RESEARCH & EXPERIMENTAL
最新[2023]版:
Q1 MEDICINE, RESEARCH & EXPERIMENTAL

影响因子: 最新[2023版] 最新五年平均 出版当年[2015版] 出版当年五年平均 出版前一年[2014版] 出版后一年[2016版]

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第一作者机构: [1]Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Department of Immunology and Microbiology, Shanghai Institute of Immunology, Shanghai Jiao Tong University School of Medicine (SJTU-SM), Shanghai, China
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通讯机构: [1]Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Department of Immunology and Microbiology, Shanghai Institute of Immunology, Shanghai Jiao Tong University School of Medicine (SJTU-SM), Shanghai, China [6]Guangdong Provincial Hospital of Chinese Medicine, Guangdong Provincial Academy of Chinese Medical Sciences, The Second Clinical School of Guangzhou University of Chinese Medicine, Guangzhou, China [7]Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Shanghai Jiao Tong University School of Medicine (SJTU-SM), Shanghai, China
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