ArticleNature communications2025
IL-17a induces age-related olfactory dysfunction by impairing regeneration and promoting respiratory metaplasia in mice.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Construction ofiScience · 2026Article
- Olfactory epithelium regeneration and homeostasis: cellular and molecular mechanisms and novel methodological advances.Cell regeneration (London, England) · 2026Review
- The microbiota-metabolite-immune axis in the olfactory cleft microenvironment: mechanisms and therapeutic implications for dysbiosis-driven olfactory dysfunction in chronic rhinosinusitis.Frontiers in immunology · 2026Review
- Mechanical constraints on cell plasticity: insights from the olfactory epithelium.Frontiers in cell and developmental biology · 2026Review
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Authors and funding
12 authors.
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Abstract
The olfactory epithelium (OE) undergoes life-long renewal and regeneration. This process is supported by the globose basal cells (GBC) during the homeostatic state, as well as horizontal basal cells (HBC) during severe damage. Inflamm-aging refers to the low-grade, chronic and progressive state of heightened pro-inflammation associated with aging. However, the impact of inflamm-aging on OE homeostasis, regeneration, and the inflammatory microenvironment is not fully understood. In this study using mouse models, we elucidate the role of interleukin-17a (IL-17a) in OE regeneration and olfactory function. Our findings implicate that inflamm-aging in aged OE promotes the recruitment and activation of immune cells, accompanied by crosstalk between HBC and T cells. Elevated expression of IL-17a in aged OE triggers inflammatory signals and impairs olfactory function. Administration of IL-17a inhibitor Y-320 or neutralizing antibody promotes sensory neuronal regeneration and reverses age-related respiratory metaplasia in OE. Co-culturing mouse OE organoids with Th17 cells impairs neuronal generation and enhances the transformation towards respiratory cells, while neutralizing antibody against IL-17a alleviates neuronal loss and respiratory transformation. Additionally, conditional knockout of IL-17a in T cells facilitates OE regeneration by promoting HBC recruitment and differentiation into GBC. Collectively, our study identifies a function of IL-17a in OE regeneration and age-related deficits in olfactory function, providing evidence for further investigation of IL-17a as a possible therapeutic target against presbyosmia.
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