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TEX264 suppresses antiviral immune response by promoting STING degradation through ER-phagy
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DOI：10.1111/febs.70541.png)
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Abstract
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Stimulator of interferon response cGAMP interactor (STING), the central transducer of the cGAS-STING signaling axis, governs type I interferon (IFN-I) production that is essential for antiviral innate immunity. Modulating STING activity and stability offers potential therapeutic strategies for viral and autoimmune diseases. Here, we demonstrate that testis-expressed protein 264 (TEX264), an endoplasmic reticulum-selective autophagy (ER-phagy) receptor, shows upregulated expression following Herpes simplex virus 1 (HSV-1) infection. Overexpression of TEX264 inhibits the activation of IFN-I signaling triggered by HSV-1 or poly(dA:dT), and enhances HSV-1 replication. Mechanistically, TEX264 interacts with WIPI2 to induce ER-phagy, leading to the degradation of STING and the negative regulation of the IFN-I response. Our findings position TEX264 as a critical regulator of the innate immune response to DNA viruses.
Keywords:
ER-phagy
HSV-1
IFN-I
STING
TEX264
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