ArticleAsian Pacific journal of allergy and immunology2017
Activation of dengue virus-specific T cells modulates vascular endothelial growth factor receptor 2 expression.
Article in Asian Pacific journal of allergy and immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed, 13 citations in OpenAlex.
- Chikungunya virus infection in the skin: histopathology and cutaneous immunological response.Frontiers in microbiology · 2025Article
- VEGF-A enhances the cytotoxic function of CD4Journal of translational medicine · 2023Article
- Current Understanding of the Role of T Cells in Chikungunya, Dengue and Zika Infections.Viruses · 2022Review
- [Value of sTREM-1 in serum and bronchoalveolar lavage fluid, APACHE II score, and SOFA score in evaluating the conditions and prognosis of children with severe pneumonia].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2020Article
- Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundThe pathogenic mechanisms underlying the increased vascular permeability in dengue hemorrhagic fever (DHF) are not well understood. Enhanced cellular immune activation, especially activation of serotype-cross reactive T cells, has been implicated in plasma leakage in DHF. Changes in several biological markers and mediators including cytokines, chemokines, angiogenic factors and their receptors have been shown to correlate with disease severity. A decline in plasma levels of a soluble form of vascular endothelial growth factor receptor 2 (VEGFR2), a receptor of vascular endothelial growth factor (VEGF), has been associated with plasma leakage in dengue patients.
objectiveWe aimed to investigate the effect of dengue virus (DV)-specific CD8⁺ T cells on the expression of VEGFR2 on endothelial cells.
methodsAn in vitro model was developed in which dengue virus-specific CD8⁺ T cells generated from peripheral blood mononuclear cells (PBMCs) of DHF patients were co-cultured with antigen-presenting cells, human umbilical vein endothelial cells (HUVECs) and activated with DV non-structural protein 3 (NS3) peptides. The expression of VEGFR2 by endothelial cells was measured.
resultsDV-specific CD8⁺ T cells were serotype cross-reactive. Activation of DV-specific CD8⁺ T cells resulted in down-regulation of soluble VEGFR2 production and an up-regulation of cell-associated VEGFR2.
conclusionsOur findings indicate that activation of DV-specific T cell is associated with modulation of VEGFR2 expression that may contribute to increased VEGF responsiveness and vascular permeability.
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