Immunological Mechanisms in Chronic Rhinosinusitis

Chronic rhinosinusitis (CRS) encompasses a spectrum of persistent sinonasal inflammatory disorders distinguished by the presence or absence of nasal polyps and by underlying immune endotypes. At its core lies an interplay between epithelial barrier dysfunction, dysregulated innate immunity and tailored adaptive responses. In polyp‐forming CRS, a type 2 immune polarisation predominates, driven by interleukin-4, ‑5 and ‑13, with pronounced eosinophil recruitment, innate lymphoid cell type 2 activation and local immunoglobulin E production. In contrast, non-polyp CRS often exhibits neutrophil-rich, type 1 or type 3 patterns with interferon-γ and interleukin-17 signatures. Tissue remodelling is orchestrated by transforming growth factor-β pathways and fibroblast activation, while recent evidence implicates metabolic shifts—particularly enhanced glycolysis—in promoting cell–matrix interactions and polyp expansion. Emerging studies also reveal an autoimmune component, with locally generated autoantibodies fostering chronic mucosal injury. Globally affecting around 5 percent of the population, CRS contributes substantially to morbidity, comorbid asthma and healthcare burden. Translational advances now focus on biologics targeting cytokines, barrier-fortifying agents and metabolic modulators to restore mucosal homeostasis and prevent polyp recurrence.

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Immunological Mechanisms in Chronic Rhinosinusitis publication trend

The graph below shows the total number of articles in immunological mechanisms in chronic rhinosinusitis across all publications each year (not limited to Nature Index journals).

Technical terms

Eosinophil: Granulocytic leucocyte central to type 2 inflammatory responses and tissue remodelling.

Cytokine: Small secreted protein that mediates communication between immune cells and orchestrates inflammatory programmes.

TGF-β receptor III (TGFBR3): Coreceptor that modulates transforming growth factor-β signalling in epithelial and stromal cells.

Single-cell RNA sequencing (scRNA-seq): High-resolution technique for profiling gene expression in individual cells to unravel cellular heterogeneity.

Autoantibody: Antibody targeting self-antigens, contributing to loss of tolerance and chronic inflammation.

Glycolytic reprogramming: Metabolic shift favouring glycolysis over oxidative phosphorylation to support immune cell activation and matrix production.

References

1. MEX3B inhibits collagen production in eosinophilic nasal polyps by downregulating epithelial cell TGFBR3 mRNA stability. JCI Insight (2023).
2. Increased glycolysis and cellular crosstalk in eosinophilic chronic rhinosinusitis with nasal polyps. Frontiers in Immunology (2024).
3. Autoimmunity: A New Focus on Nasal Polyps. International Journal of Molecular Sciences (2023).
4. Mixed T Helper Cell Signatures In Chronic Rhinosinusitis with and without Polyps. PLOS ONE (2014).
5. Antibodies and superantibodies in patients with chronic rhinosinusitis with nasal polyps. Journal of Allergy and Clinical Immunology (2016).
6. Local Immunoglobulin E in nasal polyps: Role and modulation. Frontiers in Immunology (2022).