ArticleJournal of biomedical science2009
STAT2 hypomorphic mutant mice display impaired dendritic cell development and antiviral response.
Article in Journal of biomedical science, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- Viral infections in humans and mice with genetic deficiencies of the type I IFN response pathway.European journal of immunology · 2021Review
- Stat2 stability regulation: an intersection between immunity and carcinogenesis.Experimental & molecular medicine · 2020Review
- Molecular regulation of dendritic cell development and function in homeostasis, inflammation, and cancer.Molecular immunology · 2019Review
- Fine-Tuning of Type I Interferon Response by STAT3.Frontiers in immunology · 2019Review
- STAT Family Protein Expression and Phosphorylation State during moDC Development Is Altered by Platinum-Based Chemotherapeutics.Journal of immunology research · 2019Article
- Interferon priming is essential for human CD34+ cell-derived plasmacytoid dendritic cell maturation and function.Nature communications · 2018Article
- STAT2 Is Required for TLR-Induced Murine Dendritic Cell Activation and Cross-Presentation.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- STAT2/IRF9 directs a prolonged ISGF3-like transcriptional response and antiviral activity in the absence of STAT1.The Biochemical journal · 2015Article
- Efficient Generation of Plasmacytoid Dendritic Cell from Common Lymphoid Progenitors by Flt3 Ligand.PloS one · 2015Article
- Host STAT2/type I interferon axis controls tumor growth.International journal of cancer · 2015Article
- STAT1β is not dominant negative and is capable of contributing to gamma interferon-dependent innate immunity.Molecular and cellular biology · 2014Article
- Genetic manipulation of the ApoF/Stat2 locus supports an important role for type I interferon signaling in atherosclerosis.Atherosclerosis · 2014Article
- Inducible, dose-adjustable and time-restricted reconstitution of STAT1 deficiency in vivo.PloS one · 2014Article
- A type I IFN-Flt3 ligand axis augments plasmacytoid dendritic cell development from common lymphoid progenitors.The Journal of experimental medicine · 2013Article
- STAT2 deficiency and susceptibility to viral illness in humans.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- The role of signal transducer and activator of transcription-2 in the interferon response.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2012Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interferons (IFNs) are key regulators for both innate and adaptive immune responses. By screening ENU-mutagenized mice, we identified a pedigree- P117 which displayed impaired response to type I, but not type II, IFNs. Through inheritance test, genetic mapping and sequencing, we found a T to A point mutation in the 5' splice site of STAT2 intron 4-5, leading to cryptic splicing and frame shifting. As a result, the expression of STAT2 protein was greatly diminished in the mutant mice. Nonetheless, a trace amount of functional STAT2 protein was still detectable and was capable of inducing, though to a lesser extent, IFNalpha-downstream gene expressions, suggesting that P117 is a STAT2 hypomorphic mutant. The restoration of mouse or human STAT2 gene in P117 MEFs rescued the response to IFNalpha, suggesting that the mutation in STAT2 is most likely the cause of the phenotypes seen in the pedigree. Development of different subsets of lymphocytes appeared to be normal in the mutant mice except that the percentage and basal expression of CD86 in splenic pDC and cDC were reduced. In addition, in vitro Flt3L-dependent DC development and TLR ligand-mediated DC differentiation were also defective in mutant cells. These results suggest that STAT2 positively regulates DC development and differentiation. Interestingly, a severe impairment of antiviral state and increased susceptibility to EMCV infection were observed in the mutant MEFs and mice, respectively, suggesting that the remaining STAT2 is not sufficient to confer antiviral response. In sum, the new allele of STAT2 mutant reported here reveals a role of STAT2 for DC development and a threshold requirement for full functions of type I IFNs.
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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.