Pitabut, Nada

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Pitabut, Nada
Alternative Name
Pitabut, N.
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nada.pi@kmitl.ac.th

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    Item type:Publication,
    Anti-DENV IgE correlates with dengue severity and triggers FcεRI-dependent basophil activation inhibited by Omalizumab
    (2026-12-01)
    Chan-in, Wilawan
    ;
    Vacharathit, Vimvara
    ;
    Tancharoen, Walairat
    ;
    Duangchinda, Thaneeya
    ;
    Mongkolsapaya, Juthathip
    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.