Chronic Rhinosinusitis with Nasal Polyps: T-Cell Dysregulation and Regulatory T-Cell Dysfunction
6 affiliations
- 1Sinonasal and Skull Base Tumor Section, Surgical Oncology Program (SOP), Center for Cancer Research (CCR), National Cancer Institute (NCI), National Institutes of Health (NIH), Johns Hopkins University School of Medicine, Bethesda, MD USA
- 2Department of Otolaryngology–Head and Neck Surgery, Johns Hopkins University School of Medicine, Baltimore, MD USA
- 3Sinonasal and Olfaction Program, National Institute on Deafness and Other Communication Disorders (NIDCD), National Institutes of Health, Bethesda, MD USA
- 4Department of Otolaryngology–Head and Neck Surgery, Emory University School of Medicine, Emory University, Atlanta, GA USA
- 5Department of Neurosurgery, Johns Hopkins University School of Medicine, Baltimore, MD USA
- 6Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD USA
Abstract
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 (Tregs) 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⁺ Treg 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.
Related
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- Oxidative Stress in Chronic Rhinosinusitis with Nasal Polyps: Pathophysiological Mechanisms, Biomarkers, and Therapeutic Implications
- Cross-Cultural Adaptation and Initial Psychometric Evaluation of the Kazakh-Language Sino-Nasal Outcome Test-22 (SNOT-22) in Patients with Chronic Rhinosinusitis with Nasal Polyps
BibTeX
@article{farashi2026chronic,
title = {{Chronic Rhinosinusitis with Nasal Polyps: T-Cell Dysregulation and Regulatory T-Cell Dysfunction}},
author = {Ebrahim Farashi and Tolani F. Olonisakin and Joshua M. Levy and Nyall R. London},
journal = {Current Otorhinolaryngology Reports},
year = {2026},
month = oct,
doi = {10.1007/s40136-026-00556-w},
url = {https://doi.org/10.1007/s40136-026-00556-w},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Chronic Rhinosinusitis with Nasal Polyps: T-Cell Dysregulation and Regulatory T-Cell Dysfunction
AU - Ebrahim Farashi
AU - Tolani F. Olonisakin
AU - Joshua M. Levy
AU - Nyall R. London
PY - 2026
DA - 2026/10/29
JO - Current Otorhinolaryngology Reports
DO - 10.1007/s40136-026-00556-w
UR - https://doi.org/10.1007/s40136-026-00556-w
AB - 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 (Tregs) 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⁺ Treg 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.
SN - 2167-583X
ER -