内部收益率3
生物
特里夫
干扰素调节因子
TLR3型
先天免疫系统
干扰素
干扰素基因刺激剂
转录因子
信号转导
细胞生物学
分子生物学
病毒学
受体
基因
Toll样受体
遗传学
作者
Qingfei Li,Mengjiao Wu,Kun Cui,Si Zhu,Kangsen Mai,Qinghui Ai
标识
DOI:10.1016/j.fsi.2020.05.066
摘要
Fish tend to rely more on their innate immunity to executing defense against viral infection by inducing antiviral gene production. However, the expression pattern and underlying mechanism of fish antiviral responses have yet to be fully defined. In the present study, an in vitro viral infection model was established by exposing head kidney-derived macrophages of large yellow croaker to virus analog, poly(I:C). Transcriptome analysis indicated that poly(I:C) appeared to induce potent antiviral activity featuring dominant interferon a3 (IFNa3) expression through activation of toll-like receptors (TLRs)/TIR-domain-containing adapter-inducing interferon-β (TRIF) and retinoic acid-inducible gene I-like receptors (RLRs)/mitochondrial antiviral signaling protein (MAVS) pathways. Inhibition of nuclear factor κB (NF-κB) and stimulator of interferon genes (STING)/interferon regulatory factor 3 (IRF3) pathways diminished the expression of IFNa3. Mechanistically, transcription factors including p65 and IRF3 could promote expression of IRF3, and activated IRF3 alone further increased the transcriptional activity of IFNa3. We also characterized the promoter of IFNa3 with direct IRF3 binding site which was sufficient to render the transcription of IFNa3. This effect was attenuated after deletion or mutation of the IRF3 binding sites. Taken together, our findings illustrate the distinct transcriptional profiling of fish macrophages triggered by poly(I:C). Also, this work provides new insights into the molecular mechanism underpinning coordinated activation of pathogen recognition and signaling transduction in the antiviral responses of non-model fish species.
科研通智能强力驱动
Strongly Powered by AbleSci AI