From Tregs to tissue remodelling: FOXP3 and IL-35 in the inflammatory landscape of nasal polyps.

OBJECTIVE

Inflammatory nasal polyps (NPs) are a chronic condition of the nasal mucosa linked with prolonged airway obstruction, frequent infections, and immune dysregulation. While the exact mechanisms underlying NP development remain unknown, new research indicates that immune-regulatory pathways are essential. Forkhead box P3 (FOXP3) and Interleukin-35 (IL-35) have attracted much interest.

METHODS

In this narrative review, we examine how regulatory T cells (Tregs) release the potent immunosuppressive cytokine IL-35, suppressing effector T cell responses and encouraging Treg proliferation. Studies have shown that IL-35 is essential for preserving immunological homeostasis. FOXP3, a crucial transcription factor necessary for the development and maintenance of developing and maintaining immunological tolerance, controls the development and activity of Tregs. The pathophysiology of NPs is also included in this review, along with pertinent immunological indicators linked to the advancement of the condition.

RESULT: The balance between inflammatory and regulatory responses is upset in NP patients due to dysregulation of IL-35 and FOXP3, exacerbating chronic inflammation. Studying how they interact offers novel insight into the pathophysiology of NP and identifies potential curative approaches, such as Treg regulation and IL-35 supplementation. Parallel to this, pharmacological treatments such as corticosteroids and biologics (such as dupilumab) aim to reduce type 2 inflammation.

CONCLUSION

FOXP3 and IL-35 play an important role in maintaining immunological homeostasis, and their dysregulation is associated with the persistent inflammation seen in NPs. Relying on these regulatory mechanisms may represent a promising therapeutic direction, although further experimental and clinical validation is required beyond existing anti-inflammatory therapies. Further investigation is necessary to confirm their clinical relevance.