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Investigation reveals diminished type 2 cytokine patterns during sustained inflammation in allergic rhinitis, suggesting alternative pathways.
BACKGROUND: Seasonal allergic rhinitis (SAR) is viewed as a type 2 (T2) disease driven by the IL-5/IL-5 receptor α (IL-5Rα) and IL-4/IL-13/IL-4 receptor (IL-4R) pathways and the upstream epithelial alarmins IL-33 and TSLP. However, the dynamics and expression patterns of T2-immunity in the nasal mucosa during sustained allergen exposure remain poorly understood. AIM/OBJECTIVE: To investigate whether traditional T2-cytokine and alarmin expressions persist during sustained, well-developed eosinophilic inflammation in patients with SAR. METHODS: hybridisation, and computerized image analysis to quantify immune cells, cytokine/alarmin-expression, and their receptors, focusing on IL-5Rα. RESULTS: cells were identified. IL-33 expression remained robust but was lower compared with post-seasonal observations. CONCLUSIONS AND SIGNIFICANCE: Sustained eosinophilic inflammation in SAR may be maintained by non-T2-pathways in established allergic disease, potentially informing future treatment strategies.
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Nordström et al. (2026) studied this question.
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