ReviewJournal of inflammation research2024
Atopic Dermatitis Immune Dysregulation as Dengue Predisposing Factor.
Review in Journal of inflammation research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- Roles of non-structural protein 1 in dengue virus replication and immunomodulation in vivo.The Journal of veterinary medical science · 2026Article
- Contribution of Immune Responses toJournal of inflammation research · 2026Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: The immune response is important in dengue's clinical manifestation, and the immune dysregulation in Atopic Dermatitis (AD) can permit immune evasion by viruses. There have been many studies describing the immune response in AD and the pathomechanism of dengue, but AD as a predisposing factor for dengue and its severity have not been much discussed. This review investigates how immune dysregulation in AD may be a predisposing factor for Dengue and its severe outcomes. Methods: We conducted a comprehensive analysis of studies from the past decade, focusing on dendritic cells (DCs), macrophages, mast cells (MCs), Innate Lymphoid Cell 2 (ILC-2), Natural Killer (NK) cells, interferon (IFN), interleukin (IL) 4, IL-13, and T helper (Th) 2 in AD patients with healthy subject as a comparison, using databases PubMed, Science Direct, and Google Scholar. Results: We got 44 articles that met inclusion criteria. From those articles, we resumed that moderate and severe AD patients' immune profiles showed increased DC, MCs, M2 macrophage, NK cells, and ILC2 in the lesional and non-lesional skin, decreased DC and NK cells in peripheral blood, alteration cytotoxicity of NK cells, Th2-skewed adaptive immune response in lesional and non-lesional skin, and peripheral blood. Increased DC, M2 macrophage, and MCs provide target cells for Dengue virus (DENV) replication. Alteration cytotoxicity of NK cells, ILC2, and Th2 skewed immune response facilitated immune evasion by DENV. Conclusion: The innate and adaptive immune dysregulation in moderate and severe AD provides DENV target cells and facilitates virus immune evasion that can be a predisposing factor for dengue and severe dengue. Further research is recommended to clarify the association between AD and the incidence of dengue and severe dengue because this can be a consideration in determining the prognosis and management of Dengue.
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