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Peer-reviewedCC BYFrontiers in allergy

Low-density neutrophil subsets in allergic rhinitis: heterogeneity and an emerging hypothesis for the non-type 2 endotype

  • Pengyuan Yu1
  • Feihu Wu2
  • Yufeng Chen3
  • Yun Li3
  • Xinyue Zhang3
  • Yan Ruan4
  • Gang Liu3
  • Xinyu Han4
4 affiliations
  1. 1Jiaxing Hospital of Traditional Chinese Medicine , , ,
  2. 2Shuguang Anhui Hospital Affiliated to Shanghai University of Traditional Chinese Medicine , , ,
  3. 3The First Affiliated Hospital of Anhui University of Chinese Medicine , , ,
  4. 4The First Affiliated Hospital of Guangzhou University of Chinese Medicine , , ,
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Abstract

Allergic rhinitis (AR) is conventionally viewed through a type 2/eosinophil-centric lens, yet a substantial subgroup of patients exhibits a neutrophil-predominant, corticosteroid-refractory inflammatory phenotype that responds poorly to standard therapy. Once regarded as a homogeneous, terminally differentiated lineage, neutrophils are now recognized as a functionally heterogeneous population. Among their subsets, low-density neutrophils (LDNs)—encompassing pro-inflammatory low-density granulocytes and immunosuppressive polymorphonuclear myeloid-derived suppressor cells—have emerged as key regulators of innate and adaptive immunity. This Mini Review synthesizes current evidence and proposes an emerging hypothesis that LDN heterogeneity may contribute to, rather than define, the non-type 2 endotype of AR. We discuss (i) the identification and dual functionality of LDNs; (ii) AR-specific findings, including CD16/CD62L-defined neutrophil subsets and recently described circulating LOX-1 + neutrophils that activate T cells; (iii) the neutrophil-T cell crosstalk that may amplify non-type 2 inflammation; and (iv) the translational potential of LDNs as biomarkers and therapeutic targets. A tighter characterization of LDN subsets may enable endotype-guided, neutrophil-directed therapy in AR.

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Cite

BibTeXRIS
BibTeX
@article{yu2026lowdensity,
  title = {{Low-density neutrophil subsets in allergic rhinitis: heterogeneity and an emerging hypothesis for the non-type 2 endotype}},
  author = {Pengyuan Yu and Feihu Wu and Yufeng Chen and Yun Li and Xinyue Zhang and Yan Ruan and Gang Liu and Xinyu Han},
  journal = {Frontiers in allergy},
  year = {2026},
  month = oct,
  doi = {10.3389/falgy.2026.1934796},
  url = {https://europepmc.org/article/PMC/PMC13725145},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Low-density neutrophil subsets in allergic rhinitis: heterogeneity and an emerging hypothesis for the non-type 2 endotype
AU  - Pengyuan Yu
AU  - Feihu Wu
AU  - Yufeng Chen
AU  - Yun Li
AU  - Xinyue Zhang
AU  - Yan Ruan
AU  - Gang Liu
AU  - Xinyu Han
PY  - 2026
DA  - 2026/10/19
JO  - Frontiers in allergy
DO  - 10.3389/falgy.2026.1934796
UR  - https://europepmc.org/article/PMC/PMC13725145
AB  - Allergic rhinitis (AR) is conventionally viewed through a type 2/eosinophil-centric lens, yet a substantial subgroup of patients exhibits a neutrophil-predominant, corticosteroid-refractory inflammatory phenotype that responds poorly to standard therapy. Once regarded as a homogeneous, terminally differentiated lineage, neutrophils are now recognized as a functionally heterogeneous population. Among their subsets, low-density neutrophils (LDNs)—encompassing pro-inflammatory low-density granulocytes and immunosuppressive polymorphonuclear myeloid-derived suppressor cells—have emerged as key regulators of innate and adaptive immunity. This Mini Review synthesizes current evidence and proposes an emerging hypothesis that LDN heterogeneity may contribute to, rather than define, the non-type 2 endotype of AR. We discuss (i) the identification and dual functionality of LDNs; (ii) AR-specific findings, including CD16/CD62L-defined neutrophil subsets and recently described circulating LOX-1 + neutrophils that activate T cells; (iii) the neutrophil-T cell crosstalk that may amplify non-type 2 inflammation; and (iv) the translational potential of LDNs as biomarkers and therapeutic targets. A tighter characterization of LDN subsets may enable endotype-guided, neutrophil-directed therapy in AR.
SN  - 2673-6101
ER  -