BMC infectious diseases · 2026
The HIF-1α-Th17/Treg axis in pediatric infectious mononucleosis: a clinical investigation of metabolic-immune dysregulation.
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Yang Pengli, Ni Huiping, Du Lingfang, Wang Meiling, Pang Gaofeng
Аннотация
BACKGROUND: Pediatric infectious mononucleosis (IM) is a systemic inflammatory syndrome typically triggered by primary Epstein-Barr virus (EBV) infection. The disease is characterized by a profound disruption of immune homeostasis, which can be characterized by the balance between pro-inflammatory Th17 cells and suppressive Treg cells. While hypoxia-inducible factor-1α (HIF-1α) is known to direct T-cell behavior in various inflammatory conditions, its specific role in the immunopathology of IM remains largely uncharacterized. This study aims to investigate the systemic expression of HIF-1α in pediatric IM and evaluate its correlation with the Th17/Treg homeostatic axis.
METHODS: In this prospective case-control study, we enrolled pediatric patients with acute IM and healthy, age- and sex-frequency-matched controls. Peripheral blood CD4+ T-cell subsets (Th17: CD3+CD4+IL-17A+; Treg: CD3+CD4+CD25+CD127low) were quantified via multi-color flow cytometry. Systemic levels of HIF-1α, IL-17A, and TGF-β1 were determined by enzyme-linked immunosorbent assay (ELISA). The relationship between metabolic stabilization and immune phenotype was evaluated using Spearman correlation analysis.
RESULTS: The final analysis included 40 IM patients and 37 healthy controls. Compared to the controls, IM patients exhibited a significant systemic accumulation of HIF-1α (p < 0.001) and IL-17A concentrations (p = 0.008), alongside a marked expansion of Th17 cells (p < 0.001) and a significant increase in the Th17/Treg ratio (p < 0.001). Conversely, the IM cohort experienced significantly depletions in Treg frequencies (p < 0.001) and TGF-β1 levels (p = 0.005). Correlation analysis revealed that serum HIF-1α was correlated significantly positively with Th17 frequency, the Th17/Treg ratio, and IL-17A levels and significantly negatively with Treg frequency and TGF-β1 levels.
CONCLUSIONS: Our findings reveal a significant systemic stabilization of HIF-1α in pediatric IM patients, which reflects an immunometabolic signature associated with the acute viral response. The significant correlation between HIF-1α and the shift in T-cell subsets suggests that HIF-1α may be seen as systemic sensor of disease severity in EBV infection. The results provide a theoretical foundation for targeting metabolic pathways to restore immune homeostasis in hyper-inflammatory viral diseases.
METHODS: In this prospective case-control study, we enrolled pediatric patients with acute IM and healthy, age- and sex-frequency-matched controls. Peripheral blood CD4+ T-cell subsets (Th17: CD3+CD4+IL-17A+; Treg: CD3+CD4+CD25+CD127low) were quantified via multi-color flow cytometry. Systemic levels of HIF-1α, IL-17A, and TGF-β1 were determined by enzyme-linked immunosorbent assay (ELISA). The relationship between metabolic stabilization and immune phenotype was evaluated using Spearman correlation analysis.
RESULTS: The final analysis included 40 IM patients and 37 healthy controls. Compared to the controls, IM patients exhibited a significant systemic accumulation of HIF-1α (p < 0.001) and IL-17A concentrations (p = 0.008), alongside a marked expansion of Th17 cells (p < 0.001) and a significant increase in the Th17/Treg ratio (p < 0.001). Conversely, the IM cohort experienced significantly depletions in Treg frequencies (p < 0.001) and TGF-β1 levels (p = 0.005). Correlation analysis revealed that serum HIF-1α was correlated significantly positively with Th17 frequency, the Th17/Treg ratio, and IL-17A levels and significantly negatively with Treg frequency and TGF-β1 levels.
CONCLUSIONS: Our findings reveal a significant systemic stabilization of HIF-1α in pediatric IM patients, which reflects an immunometabolic signature associated with the acute viral response. The significant correlation between HIF-1α and the shift in T-cell subsets suggests that HIF-1α may be seen as systemic sensor of disease severity in EBV infection. The results provide a theoretical foundation for targeting metabolic pathways to restore immune homeostasis in hyper-inflammatory viral diseases.