期刊
JOURNAL OF IMMUNOLOGY
卷 209, 期 10, 页码 2022-2032出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.2200013
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资金
- National Natural Science Foundation of China [32022085/31930113]
- National Key Research and Development Program of China [2018YFD0900600/2018YFD0900500]
- Independent Research and Development Projects of Maoming Laboratory [2021ZZ007/2021TDQD004]
- Southern Marine Science and Engineering Guangdong Laboratory (Zhuhai) [SML2021SP301]
- Key-Area Research and Development Program of Guangdong Province [2018B020204001]
- Fundamental Research Funds for the Central Universities, Sun Yat-sen University [22lglj05]
The activation of aryl hydrocarbon receptor (AhR) leads to increased apoptosis and restricts virus replication in shrimp infected with white spot syndrome virus. This study provides evidence for a direct link between AhR signaling and caspase-mediated apoptosis signaling.
The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor that mediates immune modulation following exposure of animals to many environmental xenobiotics. However, its role in innate immune responses during viral infection is not fully understood, especially in invertebrates. In this study, a cDNA encoding an AhR homolog was cloned from an arthropod Litopenaeus vannamei (LvAhR). The expression of LvAhR was strongly upregulated in response to the challenge of white spot syndrome virus, a pathogen of highly contagious and fatal infectious disease of shrimp. The relevance of LvAhR to host defense was underlined by heightened susceptibility and elevated virus loads after AhR-silenced shrimp exposure to white spot syndrome virus. LvAhR could induce an apoptosis response through regulating the expression of L. vannamei caspase-1 (homologous to human caspase-3) by directly targeting its promoter that was required to couple with AhR nuclear translocator. Additionally, knockdown of L. vannamei caspase-1 resulted in elevated virus titers and a lower cell apoptotic rate. Thus, we demonstrate that an AhR-caspase axis restrains virus replication by promoting antiviral apoptosis, supporting a previously unidentified direct link between AhR signaling and caspase-mediated apoptosis signaling and, furthermore, suggests that the AhR-caspase axis could be a potential therapeutic target for enhancing antiviral responses in arthropods.
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