Cellular microenvironments critically control the activation of innate immune responses. N-chlorotaurine (Tau-Cl) is an endogenous metabolite that is markedly produced and secreted during pathogenic invasion. However, its effect on the antiviral innate immune responses remains unclear. Here, we demonstrate that viral infection upregulates cellular Tau-Cl level. Tau-Cl attenuates viral infection-induced expression of type I IFNs and facilitates viral replication both in vitro and in vivo. Mechanistically, Tau-Cl facilitates the oxidation of IRF3 at Cys222 and Cys371, a key transcription factor that governs the transcription of type I IFNs. Tau-Cl inhibits phosphorylation and nuclear translocation of IRF3, and blocks IRF3 binding to the IFN-β promoter region. Therefore, we identify Tau-Cl as an endogenous suppressor of IRF3-driven antiviral innate responses and uncover an immune escape mechanism of viruses by affecting host microenvironments.
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