ArticlePLoS pathogens2019
Type I interferon-dependent CCL4 is induced by a cGAS/STING pathway that bypasses viral inhibition and protects infected tissue, independent of viral burden.
Article in PLoS pathogens, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 26 citations in OpenAlex.
- Acute and lifelong exercise modulate the tumorigenic potential of human lung cancer cells and their susceptibility to cisplatin.Experimental physiology · 2026Article
- Marine Bromophenol Derivatives as a Novel Class of Potent Small-Molecule STING Agonists.Current issues in molecular biology · 2026Article
- MPXV infection activates cGAS-STING signaling and IFN-I treatment reduces pathogenicity of mpox in CAST/EiJ mice and rhesus macaques.Cell reports. Medicine · 2025Article
- Article
- T Cell Surveillance during Cutaneous Viral Infections.Viruses · 2024Review
- Transcriptomic alterations in cortical astrocytes following the development of post-traumatic epilepsy.Scientific reports · 2024Article
- γδ T Cells Mediate a Requisite Portion of a Wound Healing Response Triggered by Cutaneous Poxvirus Infection.Viruses · 2024Article
- Cross-presenting Langerhans cells are required for the early reactivation of resident CD8Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- STING Agonist-Derived LNP-mRNA Vaccine Enhances Protective Immunity Against SARS-CoV-2.Nano letters · 2023Article
- CCL4 participates in the reprogramming of glucose metabolism induced by ALV-J infection in chicken macrophages.Frontiers in microbiology · 2023Article
- Epigenetic Repression of STING by MYC Promotes Immune Evasion and Resistance to Immune Checkpoint Inhibitors in Triple-Negative Breast Cancer.Cancer immunology research · 2022Article
- An increase in glycoprotein concentration on extracellular virions dramatically alters vaccinia virus infectivity and pathogenesis without impacting immunogenicity.PLoS pathogens · 2021Article
- Bifurcated monocyte states are predictive of mortality in severe COVID-19.bioRxiv : the preprint server for biology · 2021Article
- Interferon Lambda Signaling in Macrophages Is Necessary for the Antiviral Response to Influenza.Frontiers in immunology · 2021Article
- Integrative Transcriptomic Analysis Reveals the Immune Mechanism for a CyHV-3-Resistant Common Carp Strain.Frontiers in immunology · 2021Article
- Cyclic GMP-AMP synthase promotes the inflammatory and autophagy responses in Huntington disease.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Vaccinia Virus Activation and Antagonism of Cytosolic DNA Sensing.Frontiers in immunology · 2020Review
- Potential mechanism prediction of Cold-Damp Plague Formula against COVID-19 via network pharmacology analysis and molecular docking.Chinese medicine · 2020Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Type I interferons (T1-IFN) are critical in the innate immune response, acting upon infected and uninfected cells to initiate an antiviral state by expressing genes that inhibit multiple stages of the lifecycle of many viruses. T1-IFN triggers the production of Interferon-Stimulated Genes (ISGs), activating an antiviral program that reduces virus replication. The importance of the T1-IFN response is highlighted by the evolution of viral evasion strategies to inhibit the production or action of T1-IFN in virus-infected cells. T1-IFN is produced via activation of pathogen sensors within infected cells, a process that is targeted by virus-encoded immunomodulatory molecules. This is probably best exemplified by the prototypic poxvirus, Vaccinia virus (VACV), which uses at least 6 different mechanisms to completely block the production of T1-IFN within infected cells in vitro. Yet, mice lacking aspects of T1-IFN signaling are often more susceptible to infection with many viruses, including VACV, than wild-type mice. How can these opposing findings be rationalized? The cytosolic DNA sensor cGAS has been implicated in immunity to VACV, but has yet to be linked to the production of T1-IFN in response to VACV infection. Indeed, there are two VACV-encoded proteins that effectively prevent cGAS-mediated activation of T1-IFN. We find that the majority of VACV-infected cells in vivo do not produce T1-IFN, but that a small subset of VACV-infected cells in vivo utilize cGAS to sense VACV and produce T1-IFN to protect infected mice. The protective effect of T1-IFN is not mediated via ISG-mediated control of virus replication. Rather, T1-IFN drives increased expression of CCL4, which recruits inflammatory monocytes that constrain the VACV lesion in a virus replication-independent manner by limiting spread within the tissue. Our findings have broad implications in our understanding of pathogen detection and viral evasion in vivo, and highlight a novel immune strategy to protect infected tissue.
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