ArticleProceedings of the National Academy of Sciences of the United States of America2025
Induction of the ISR by AB5 subtilase cytotoxin drives type-I IFN expression in pDCs via STING activation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- VPS34-IN1 potentiates STING-dependent activation in human CAL-1 cells.Cellular & molecular biology letters · 2026Article
- Induction of the ISR by AB5 subtilase cytotoxin drives type-I IFN expression in pDCs via STING activation.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
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Authors and funding
30 authors.
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Abstract
We demonstrate that exposure to the AB5 subtilase cytotoxin (SubAB) induces the unfolded protein response (UPR) in human peripheral blood mononuclear cells, concomitant with a proinflammatory response across distinct cell subsets. Notably, SubAB selectively induces type-I interferon (IFN) expression in plasmacytoid dendritic cells, acting synergistically with Toll-like receptor 7 stimulation. The induction of type-I IFN in response to SubAB relies on stimulator of interferon genes (STING) activation, coupled with protein synthesis inhibition mediated by protein kinase R-like endoplasmic reticulum kinase (PERK) and phosphorylation of the eukaryotic translation initiation factor 2 subunit-alpha. By impeding mRNA translation through the integrated stress response, SubAB precipitates the downregulation of the negative innate signaling feedback regulator Tax1-binding protein 1. This downregulation is necessary to unleash TANK-binding kinase 1 signaling associated with STING activation. These findings shed light on how UPR-inducing conditions may regulate the immune system during infection or pathogenesis.
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