ArticleProceedings of the National Academy of Sciences of the United States of America2013
Stat2 loss leads to cytokine-independent, cell-mediated lethality in LPS-induced sepsis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
27 citing papers in PubMed, 43 citations in OpenAlex.
- Restoring the FOXO1 geroprotective pathway via seno-resistant mesenchymal progenitor cells alleviates primate epididymal aging.Protein & cell · 2026Article
- STAT2 Promotes Tumor Growth in Colorectal Cancer Independent of Type I IFN Receptor Signaling.Current oncology (Toronto, Ont.) · 2025Article
- Procyanidin-B1-EnrichedAnimals : an open access journal from MDPI · 2025Article
- snRNA-seq reveals key transcription factors in the inflammatory response of microglia after intracerebral hemorrhage.Scientific reports · 2025Article
- The Dual-Edged Sword: Risks and Benefits of JAK Inhibitors in Infections.Pathogens (Basel, Switzerland) · 2025Review
- Identification of signaling networks associated with lactate modulation of macrophages and dendritic cells.Heliyon · 2025Article
- Origin recognition complex subunit 6 (ORC6) is a key mediator of LPS-induced NFκB activation and the pro-inflammatory response.Cell communication and signaling : CCS · 2024Article
- The Impact of Persistent Noise Exposure under Inflammatory Conditions.Healthcare (Basel, Switzerland) · 2023Article
- Exposing the Two Contrasting Faces of STAT2 in Inflammation.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2022Review
- Initial activation of STAT2 induced by IAV infection is critical for innate antiviral immunity.Frontiers in immunology · 2022Article
- Human Disease Phenotypes Associated with Loss and Gain of Function Mutations in STAT2: Viral Susceptibility and Type I Interferonopathy.Journal of clinical immunology · 2021Review
- Disrupting interferon-alpha and NF-kappaB crosstalk suppresses IFITM1 expression attenuating triple-negative breast cancer progression.Cancer letters · 2021Article
- Stat2-Drp1 mediated mitochondrial mass increase is necessary for pro-inflammatory differentiation of macrophages.Redox biology · 2020Article
- Stat2 stability regulation: an intersection between immunity and carcinogenesis.Experimental & molecular medicine · 2020Review
- STAT2 dependent Type I Interferon response promotes dysbiosis and luminal expansion of the enteric pathogen Salmonella Typhimurium.PLoS pathogens · 2019Article
- IRF9 and unphosphorylated STAT2 cooperate with NF-κB to drive IL6 expression.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Article
- STAT2 Is a Pervasive Cytokine Regulator due to Its Inhibition of STAT1 in Multiple Signaling Pathways.PLoS biology · 2016Article
- STAT2 Is Required for TLR-Induced Murine Dendritic Cell Activation and Cross-Presentation.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- NK cells promote neutrophil recruitment in the brain during sepsis-induced neuroinflammation.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
14 authors at 6 institutions in 2 countries.
Funding
Abstract
Deregulated Toll-like receptor (TLR)-triggered inflammatory responses that depend on NF-κB are detrimental to the host via excessive production of proinflammatory cytokines, including TNF-α. Stat2 is a critical component of type I IFN signaling, but it is not thought to participate in TLR signaling. Our study shows that LPS-induced lethality in Stat2(-/-) mice is accelerated as a result of increased cellular transmigration. Blocking intercellular adhesion molecule-1 prevents cellular egress and confers survival of Stat2(-/-) mice. The main determinant of cellular egress in Stat2(-/-) mice is the genotype of the host and not the circulating leukocyte. Surprisingly, lethality and cellular egress observed on Stat2(-/-) mice are not associated with excessive increases in classical sepsis cytokines or chemokines. Indeed, in the absence of Stat2, cytokine production in response to multiple TLR agonists is reduced. We find that Stat2 loss leads to reduced expression of NF-κB target genes by affecting nuclear translocation of NF-κB. Thus, our data reveal the existence of a different mechanism of LPS-induced lethality that is independent of NF-κB triggered cytokine storm but dependent on cellular egress.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.