ArticleImmunology2018
Interleukin-33 contributes to disease severity in Dengue virus infection in mice.
Article in Immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- IL-33 is associated with alveolar dysfunction in patients with viral lower respiratory tract disease.Mucosal immunology · 2025Article
- Anti-inflammatory effect of Faloak (Open veterinary journal · 2024Article
- Oligodendrocyte-derived IL-33 functions as a microglial survival factor during neuroinvasive flavivirus infection.PLoS pathogens · 2023Article
- Longitudinal proteomic profiling of the inflammatory response in dengue patients.PLoS neglected tropical diseases · 2023Article
- Clinical and prognostic relevance of sST2 in adults with dengue-associated cardiac impairment and severe dengue.PLoS neglected tropical diseases · 2022Article
- The Merkel Cell Polyomavirus T-Antigens and IL-33/ST2-IL1RAcP Axis: Possible Role in Merkel Cell Carcinoma.International journal of molecular sciences · 2022Article
- A murine model of dengue virus infection in suckling C57BL/6 and BALB/c mice.Animal models and experimental medicine · 2021Article
- Dengue mouse models for evaluating pathogenesis and countermeasures.Current opinion in virology · 2020Review
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Authors and funding
9 authors.
Funding
Abstract
The excessive inflammation often present in patients with severe dengue infection is considered both a hallmark of disease and a target for potential treatments. Interleukin-33 (IL-33) is a pleiotropic cytokine with pro-inflammatory effects whose role in dengue has not been fully elucidated. We demonstrate that IL-33 plays a disease-exacerbating role during experimental dengue infection in immunocompetent mice. Mice infected with dengue virus serotype 2 (DENV2) produced high levels of IL-33. DENV2-infected mice treated with recombinant IL-33 developed markedly more severe disease compared with untreated mice as assessed by mortality, granulocytosis, liver damage and pro-inflammatory cytokine production. Conversely, ST2
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