Purpose of Review Chronic rhinosinusitis with nasal polyps (CRSwNP) is a heterogeneous inflammatory disorder driven by dysregulated innate and adaptive immune responses. This review summarizes current evidence on the roles of T-helper cell subsets and regulatory T-cells (T regs ) in CRSwNP pathogenesis and discusses their implications for disease persistence and targeted therapy. Recent Findings Beyond classical Th2-driven inflammation, recent studies demonstrate important contributions from Th1, Th9, Th17, Th22, and CD8⁺ effector-memory/tissue-resident T-cells to epithelial injury, tissue remodeling, and disease recurrence. Reduced FOXP3⁺ T reg frequency and impaired function, together with alterations in IL-2, TGF-β, and IL-10 signaling, may contribute to persistent immune activation and inflammatory heterogeneity. Advances in biologic therapies targeting type 2 inflammation have substantially improved outcomes in selected patients. Summary T-cell dysregulation is central to the immunopathogenesis of CRSwNP. A better understanding of immune endotypes, T-cell plasticity, and regulatory pathways may facilitate biomarker-guided patient stratification and support the development of more precise immunomodulatory therapies.
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Farashi et al. (2026) studied this question.
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