ArticleProceedings of the National Academy of Sciences of the United States of America2001
Enhanced resistance in STAT6-deficient mice to infection with ectromelia virus.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 29 citations in OpenAlex.
- The Multifaceted Roles of STAT6: Implications for Precision Immunotherapeutics.ImmunoTargets and therapy · 2026Review
- The Dynamic Interface of Viruses with STATs.Journal of virology · 2020Review
- Type I interferon-dependent CCL4 is induced by a cGAS/STING pathway that bypasses viral inhibition and protects infected tissue, independent of viral burden.PLoS pathogens · 2019Article
- JAK/STAT Cytokine Signaling at the Crossroad of NK Cell Development and Maturation.Frontiers in immunology · 2019Review
- Article
- STATs in NK-Cells: The Good, the Bad, and the Ugly.Frontiers in immunology · 2016Review
- Fas/FasL pathway participates in regulation of antiviral and inflammatory response during mousepox infection of lungs.Mediators of inflammation · 2015Article
- Article
- Transcriptional regulation by STAT6.Immunologic research · 2011Review
- Poxvirus tropism.Nature reviews. Microbiology · 2005Review
- Polarized type 1 cytokine response and cell-mediated immunity determine genetic resistance to mousepox.Proceedings of the National Academy of Sciences of the United States of America · 2004Article
- Protective effect of exogenous recombinant mouse interferon-gamma and tumour necrosis factor-alpha on ectromelia virus infection in susceptible BALB/c mice.Clinical and experimental immunology · 2004Article
- Evidence inconsistent with a negative influence of T helper 2 cells on protection afforded by a dominant T helper 1 response against Mycobacterium tuberculosis lung infection in mice.Infection and immunity · 2002Article
- Inhibition of interferons by ectromelia virus.Journal of virology · 2002Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We inoculated BALB/c mice deficient in STAT6 (STAT6(-/-)) and their wild-type (wt) littermates (STAT6(+/+)) with the natural mouse pathogen, ectromelia virus (EV). STAT6(-/-) mice exhibited increased resistance to generalized infection with EV when compared with STAT6(+/+) mice. In the spleens and lymph nodes of STAT6(-/-) mice, T helper 1 (Th1) cytokines were induced at earlier time points and at higher levels postinfection when compared with those in STAT6(+/+) mice. Elevated levels of NO were evident in plasma and splenocyte cultures of EV-infected STAT6(-/-) mice in comparison with STAT6(+/+) mice. The induction of high levels of Th1 cytokines in the mutant mice correlated with a strong natural killer cell response. We demonstrate in genetically susceptible BALB/c mice that the STAT6 locus is critical for progression of EV infection. Furthermore, in the absence of this transcription factor, the immune system defaults toward a protective Th1-like response, conferring pronounced resistance to EV infection and disease progression.
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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.