ArticleJournal of virology2012
Mice deficient in STAT1 but not STAT2 or IRF9 develop a lethal CD4+ T-cell-mediated disease following infection with lymphocytic choriomeningitis virus.
Article in Journal of virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 49 citations in OpenAlex.
- Integrative proteomics and lipidomics reveals dual roles for lipid droplets in the host cell antiviral response.Nature communications · 2026Article
- STAT1 expression in myeloid cells restrains murine norovirus-induced hepatitis and fibrosis.bioRxiv : the preprint server for biology · 2026Article
- STAT1-Deficient HPV E6/E7-Associated Cancers Maintain Host Immunocompetency against Therapeutic Intervention.Vaccines · 2024Article
- CD8Viruses · 2024Article
- Identification of Selection Signatures and Candidate Genes Related to Environmental Adaptation and Economic Traits in Tibetan Pigs.Animals : an open access journal from MDPI · 2024Article
- The hyperinflammatory spectrum: from defects in cytotoxicity to cytokine control.Frontiers in immunology · 2023Review
- Innate immunity in rickettsial infections.Frontiers in cellular and infection microbiology · 2023Review
- 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
- Type I interferon transcriptional network regulates expression of coinhibitory receptors in human T cells.Nature immunology · 2022Article
- Restriction of Viral Replication, Rather than T Cell Immunopathology, Drives Lethality in Murine Norovirus CR6-Infected STAT1-Deficient Mice.Journal of virology · 2022Article
- Viral infections in humans and mice with genetic deficiencies of the type I IFN response pathway.European journal of immunology · 2021Review
- The Effects of Interferons on Allogeneic T Cell Response in GVHD: The Multifaced Biology and Epigenetic Regulations.Frontiers in immunology · 2021Review
- SARS-CoV-2 Spike Targets USP33-IRF9 AxisFrontiers in immunology · 2021Article
- Contribution of STAT1 to innate and adaptive immunity during type I interferon-mediated lethal virus infection.PLoS pathogens · 2020Article
- CD8 T Cells and STAT1 Signaling Are Essential Codeterminants in Protection from Polyomavirus Encephalopathy.Journal of virology · 2020Article
- Nonstructural Protein 11 of Porcine Reproductive and Respiratory Syndrome Virus Induces STAT2 Degradation To Inhibit Interferon Signaling.Journal of virology · 2019Article
- Distinct PLZFJournal of immunology (Baltimore, Md. : 1950) · 2019Article
- Zika virus encephalitis in immunocompetent mice is dominated by innate immune cells and does not require T or B cells.Journal of neuroinflammation · 2019Article
- Porcine Reproductive and Respiratory Syndrome Virus nsp11 Antagonizes Type I Interferon Signaling by Targeting IRF9.Journal of virology · 2019Article
- Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interferon (IFN) signaling is crucial for antiviral immunity. While type I IFN signaling is mediated by STAT1, STAT2, and IRF9, type II IFN signaling requires only STAT1. Here, we studied the roles of these signaling factors in the host response to systemic infection with lymphocytic choriomeningitis virus (LCMV). In wild-type (WT) mice and mice lacking either STAT2 or IRF9, LCMV infection was nonlethal, and the virus either was cleared (WT) or established persistence (STAT2 knockout [KO] and IRF9 KO). However, in the case of STAT1 KO mice, LCMV infection was lethal and accompanied by severe multiorgan immune pathology, elevated expression of various cytokine genes in tissues, and cytokines in the serum. This lethal phenotype was unaltered by the coabsence of the gamma interferon (IFN-γ) receptor and hence was not dependent on IFN-γ. Equally, the disease was not due to a combined defect in type I and type II IFN signaling, as IRF9 KO mice lacking the IFN-γ receptor survived infection with LCMV. Clearance of LCMV is mediated normally by CD8(+) T cells. However, the depletion of these cells in LCMV-infected STAT1 KO mice was delayed, but did not prevent, lethality. In contrast, depletion of CD4(+) T cells prevented lethality in LCMV-infected STAT1 KO mice and was associated with a reduction in tissue immune pathology. These studies highlight a fundamental difference in the role of STAT1 versus STAT2 and IRF9. While all three factors are required to limit viral replication and spread, only STAT1 has the unique function of preventing the emergence of a lethal antiviral CD4(+) T-cell response.
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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.