- Research Article
- 10.1038/s41598-026-43199-z
Anti-DENV IgE correlates with dengue severity and triggers FcεRI-dependent basophil activation inhibited by Omalizumab.
- Mar 19, 2026
- Scientific reports
- Wilawan Chan-In + 5 more +5
Severe dengue, marked by plasma leakage, is often linked to secondary heterotypic dengue virus (DENV) infection. While mast cells and basophils contribute to dengue pathogenesis, the role of anti-DENV IgE remains unclear. Here, we investigated whether anti-DENV IgE promotes FcεRI-dependent basophil activation, potentially contributing to disease severity. Plasma from dengue fever (DF, n = 42) and dengue hemorrhagic fever (DHF, n = 56) patients, collected at febrile, defervescence, and convalescent phases, were analyzed using an in-house IgE-capture ELISA developed to detect antibodies against all four DENV serotypes. Functional assays employed RS-ATL8, a human FcεRI-expressing basophil reporter cell line, to assess IgE-mediated activation following DENV antigen cross-linking. The anti-IgE monoclonal antibody Omalizumab was used to evaluate FcεRI dependence. Anti-DENV IgE was detected in both DF and DHF, peaking at defervescence and significantly higher in DHF. Total IgE was elevated but did not differ between groups. About one-third of anti-DENV-IgE-positive plasma samples induced RS-ATL8 activation upon DENV challenge, an effect abolished by omalizumab. These findings indicate a potential pathogenic role of anti-DENV IgE and provide a rationale for further investigation of IgE-targeted interventions.
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