Interleukin-Mediated Macrophage Polarization in Allergic Rhinitis Inflammation: A Systematic Review

Allergic rhinitis (AR) is driven by interleukin (IL) network dysregulation and imbalanced macrophage polarization. This systematic review summarizes the molecular mechanisms by which ILs regulate macrophage phenotypic switching in AR inflammation.

We screened the PubMed and Embase databases from January 2010 to January 2026 to identify published studies. The search keywords used were as follows: ["interleukin" or "IL"], ["allergic rhinitis" or "AR"], ["macrophages"] and ["inflammation"]. A total of 223 peer-reviewed studies on human/animal models were included, and articles that did not meet the requirements were excluded.

Pro-inflammatory ILs (IL-4/IL-13, IL-1β/IL-6/IL-17A) promote pathogenic M1/M2a macrophage polarization via STAT6, NF-κB and NLRP3 pathways, aggravating inflammatory responses. Anti-inflammatory ILs (IL-10, IL-27) induce M2c polarization and restore immune balance through STAT3/STAT1 signaling. Targeted interventions (dupilumab, MCC950, chlorogenic acid) effectively reverse polarization imbalance and alleviate AR symptoms. Clinically, AR patients present disrupted IL ratios, M1/M2 imbalance and impaired nasal mucosal barriers.

IL-mediated macrophage polarization is a core driver of AR inflammation. Targeting these regulatory pathways provides promising precision therapeutic strategies for AR.