Literature DB >> 21847628

Interleukin 29 enhances expression of Toll receptor 3 and mediates antiviral signals in human keratinocytes.

Sheng-Quan Zhang1, Zheng Zhang, Xin Luo, Sen Yang, Yu Chai, Hai-Liang Huang, Xian-Yong Yin, Dao-Jun Hu, Chun-Jun Yang, Jun-Lin Liu, Xue-Jun Zhang.   

Abstract

OBJECTIVE: Interleukin 29 (IL-29) is a class II cytokine and displays numerous immune functions other than its anti-viral and antiproliferation activities. This study is focused on the effect of IL-29 on human keratinocytes (KCs).
METHODS: Primary KCs were stimulated by various concentrations of IL-29 for different time periods, and antiviral proteins and TLR3 gene expression were then analyzed by real-time PCR. The signal pathways activated by IL-29 in KCs were detected by western blot. The antiviral activity of IL-29 was determined by methylthiazolyldiphenyl-tetrazolium bromide, and small interfering RNA knockdown was used to analyze the role of toll receptor 3 (TLR3) in the antiviral activity of IL-29.
RESULTS: IL-29 was able to induce expression of antiviral proteins and TLR3 gene expression in KCs. IL-29 pretreatment strongly enhanced herpes simplex virus type 1 (HSV-1)-induced expression of the interferon β (IFN-β) gene and protected the KCs from HSV-1 challenge. The IL-29 antiviral activity was partially dependent on TLR3 expression induced by this cytokine, and mechanistic studies demonstrated that the regulation of TLR3 expression by IL-29 might be partially dependent on Janus kinase /signal transducer and activator of transcription (JAK-STATs) activation.
CONCLUSION: IL-29-induced TLR3 expression is involved in antiviral activity of IL-29 in KCs, which suggests a feasible method to cure certain viral infections of the skin.

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Year:  2011        PMID: 21847628     DOI: 10.1007/s00011-011-0364-z

Source DB:  PubMed          Journal:  Inflamm Res        ISSN: 1023-3830            Impact factor:   4.575


  29 in total

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4.  Maturing dendritic cells are an important source of IL-29 and IL-20 that may cooperatively increase the innate immunity of keratinocytes.

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