Eosinophils as immunoregulatory players in allergic rhinitis: beyond cytotoxicity

This is the authors' abstract. We don't add key points for this paper.

Eosinophils have traditionally been viewed as terminal effector cells in allergic rhinitis (AR), driving tissue damage through the release of cytotoxic granule proteins and pro-inflammatory mediators. However, accumulating evidence over the past two decades has challenged this paradigm, revealing that eosinophils harbor a substantial immunoregulatory repertoire. This Mini Review synthesizes emerging findings on four underappreciated dimensions of eosinophil immunoregulatory function in the context of AR: (i) the capacity of eosinophils to produce interleukin-10 (IL-10) and engage in functional crosstalk with Foxp3+ regulatory T cells (Tregs); (ii) the dual role of eosinophil-derived transforming growth factor-beta (TGF-β) in both tissue remodeling and mucosal tolerance; (iii) eosinophil lipid mediator class-switching from pro-inflammatory cysteinyl leukotrienes (CysLTs) to specialized pro-resolving mediators (SPMs); and (iv) the functional heterogeneity between tissue-resident and inflammatory eosinophil subsets. We further discuss the clinical implications of these findings, including the paradoxical outcomes of anti-IL-5 therapies in AR and the potential of immunoregulatory eosinophil markers as biomarkers for allergen-specific immunotherapy (AIT). A deeper understanding of the context-dependent immunoregulatory functions of eosinophils in the nasal mucosa may inform precision therapeutic strategies that selectively target pro-inflammatory eosinophil subsets while preserving their homeostatic and tolerogenic roles.