tetano
Editor, Senior Moderator
Cells
. 2025 Sep 28;14(19):1511.
doi: 10.3390/cells14191511. Immunological Mechanisms Underlying Allergy Predisposition After SARS-CoV-2 Infection in Children
Filippos Filippatos[SUP] 1 [/SUP], Dimitra-Ifigeneia Matara[SUP] 1 [/SUP], Athanasios Michos[SUP] 1 [/SUP], Konstantinos Kakleas[SUP] 1 [/SUP]
Affiliations
As the pediatric COVID-19 landscape evolves, it is essential to evaluate whether SARS-CoV-2 infection predisposes children to allergic disorders. This narrative review synthesizes current epidemiological and immunological evidence linking pediatric COVID-19 with new-onset atopy. Epidemiological data remain heterogeneous: large Korean and multinational cohorts report increased risks of asthma and allergic rhinitis following COVID-19, whereas U.S. cohorts show neutral or protective associations, highlighting geographic and methodological variability. Mechanistic insights provide biological plausibility: epithelial injury and the release of alarmin cytokines (IL-33, IL-25, TSLP) promote Th2 polarization and ILC2 expansion, while epigenetic "scars" (e.g., LMAN2 methylation changes) and hematopoietic stem cell reprogramming may sustain long-term Th2 bias. Cytokine memory involving IL-7 and IL-15 contributes to altered T- and B-cell homeostasis, whereas disrupted regulatory T-cell function may reduce tolerance thresholds. Paradoxical trade-offs exist, such as ACE2 downregulation in allergic airways, which may lower viral entry but simultaneously amplify type-2 inflammation. Together, these processes suggest that SARS-CoV-2 infection could foster a pro-allergic milieu in susceptible children. Although current evidence is inconclusive, integrating epidemiological surveillance with mechanistic studies is crucial for predicting and alleviating post-COVID allergic outcomes. Longitudinal pediatric cohorts and interventions targeting epithelial alarmins or microbiome restoration may hold promise for prevention.
Keywords: COVID-19; SARS-CoV-2; allergy; cytokines; immunity.
. 2025 Sep 28;14(19):1511.
doi: 10.3390/cells14191511. Immunological Mechanisms Underlying Allergy Predisposition After SARS-CoV-2 Infection in Children
Filippos Filippatos[SUP] 1 [/SUP], Dimitra-Ifigeneia Matara[SUP] 1 [/SUP], Athanasios Michos[SUP] 1 [/SUP], Konstantinos Kakleas[SUP] 1 [/SUP]
Affiliations
- PMID: 41090740
- PMCID: PMC12523570
- DOI: 10.3390/cells14191511
As the pediatric COVID-19 landscape evolves, it is essential to evaluate whether SARS-CoV-2 infection predisposes children to allergic disorders. This narrative review synthesizes current epidemiological and immunological evidence linking pediatric COVID-19 with new-onset atopy. Epidemiological data remain heterogeneous: large Korean and multinational cohorts report increased risks of asthma and allergic rhinitis following COVID-19, whereas U.S. cohorts show neutral or protective associations, highlighting geographic and methodological variability. Mechanistic insights provide biological plausibility: epithelial injury and the release of alarmin cytokines (IL-33, IL-25, TSLP) promote Th2 polarization and ILC2 expansion, while epigenetic "scars" (e.g., LMAN2 methylation changes) and hematopoietic stem cell reprogramming may sustain long-term Th2 bias. Cytokine memory involving IL-7 and IL-15 contributes to altered T- and B-cell homeostasis, whereas disrupted regulatory T-cell function may reduce tolerance thresholds. Paradoxical trade-offs exist, such as ACE2 downregulation in allergic airways, which may lower viral entry but simultaneously amplify type-2 inflammation. Together, these processes suggest that SARS-CoV-2 infection could foster a pro-allergic milieu in susceptible children. Although current evidence is inconclusive, integrating epidemiological surveillance with mechanistic studies is crucial for predicting and alleviating post-COVID allergic outcomes. Longitudinal pediatric cohorts and interventions targeting epithelial alarmins or microbiome restoration may hold promise for prevention.
Keywords: COVID-19; SARS-CoV-2; allergy; cytokines; immunity.