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Peer-reviewedCC BY-NC-NDActa pharmaceutica Sinica. B

Mapping neutrophil membrane bioactivity to therapeutic interfaces: Biology, disease targeting, and activity-guided biomimetic therapy.

5 affiliations
  1. 1School of Pharmacy and Bioengineering, Chongqing University of Technology, Chongqing 400054, China.
  2. 2Yunnan Key Laboratory of Stem Cell and Regenerative Medicine, Rehabilitation School, Kunming Medical University, Kunming 650500, China.
  3. 3Department of Neurology, Xinqiao Hospital, The Army Medical University (Third Military Medical University), Chongqing 400033, China.
  4. 4School of Pharmacy, Kunming Medical University, Kunming 650500, China.
  5. 5Nuclear Medicine and Radiation Safety Key Laboratory of Sichuan Province, Major Disease Research & Translational Innovation Center, North Sichuan Medical College, Nanchong 637100, China.

Abstract

Neutrophil plasma membranes encode a tightly coordinated set of bioactivities that control inflammatory trafficking, endothelial adhesion under shear, effector activation, and immune regulation. In this review, we present a membrane-centric framework that conceptualizes the neutrophil membrane as a programmable therapeutic interface integrating targeting, adhesion, and effector regulation. We delineate core membrane modules-including chemokine-sensing G protein-coupled receptors (GPCRs), selectin ligands, β2 integrins, Fcγ and complement receptors, pattern-recognition receptors (PRRs), and lipid-raft microdomains-and examine how their coordinated dynamics govern tissue targeting, adhesion kinetics, effector thresholds, and resolution. Integrating evidence from infection, sterile inflammation, autoimmunity, and cancer, we highlight how dysregulated membrane programs drive pathology, while their selective tuning enables therapeutic benefit. Building on this biology, we discuss two convergent intervention strategies: direct pharmacological modulation of neutrophil membrane signaling axes, and activity-guided engineering of neutrophil membrane-derived therapeutics, including native vesicles and membrane-coated nanomaterials. We further link key engineering parameters-such as membrane orientation, ligand density, glycan architecture, and microdomain integrity-to mechanism-based potency, safety, and translational control. By positioning the neutrophil membrane as a programmable interface rather than a static biomimetic shell, this review outlines a rational roadmap for developing predictable, dose-controlled therapies for infection, inflammatory diseases, and cancer.

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BibTeX
@article{yang2026mapping,
  title = {{Mapping neutrophil membrane bioactivity to therapeutic interfaces: Biology, disease targeting, and activity-guided biomimetic therapy.}},
  author = {Qingqing Yang and Mingjing Leng and Wenbi Jiang and Huan Yang and Tong Wu and Ting Zhou and Zhennan She and Gang Xiang and Xing Zhou and Xiaohui Li},
  journal = {Acta pharmaceutica Sinica. B},
  year = {2026},
  month = aug,
  doi = {10.1016/j.apsb.2026.08.013},
  url = {https://europepmc.org/article/MED/42948691},
  note = {CC BY-NC-ND},
}
RIS
TY  - JOUR
TI  - Mapping neutrophil membrane bioactivity to therapeutic interfaces: Biology, disease targeting, and activity-guided biomimetic therapy.
AU  - Qingqing Yang
AU  - Mingjing Leng
AU  - Wenbi Jiang
AU  - Huan Yang
AU  - Tong Wu
AU  - Ting Zhou
AU  - Zhennan She
AU  - Gang Xiang
AU  - Xing Zhou
AU  - Xiaohui Li
PY  - 2026
DA  - 2026/08/26
JO  - Acta pharmaceutica Sinica. B
DO  - 10.1016/j.apsb.2026.08.013
UR  - https://europepmc.org/article/MED/42948691
AB  - Neutrophil plasma membranes encode a tightly coordinated set of bioactivities that control inflammatory trafficking, endothelial adhesion under shear, effector activation, and immune regulation. In this review, we present a membrane-centric framework that conceptualizes the neutrophil membrane as a programmable therapeutic interface integrating targeting, adhesion, and effector regulation. We delineate core membrane modules-including chemokine-sensing G protein-coupled receptors (GPCRs), selectin ligands, β2 integrins, Fcγ and complement receptors, pattern-recognition receptors (PRRs), and lipid-raft microdomains-and examine how their coordinated dynamics govern tissue targeting, adhesion kinetics, effector thresholds, and resolution. Integrating evidence from infection, sterile inflammation, autoimmunity, and cancer, we highlight how dysregulated membrane programs drive pathology, while their selective tuning enables therapeutic benefit. Building on this biology, we discuss two convergent intervention strategies: direct pharmacological modulation of neutrophil membrane signaling axes, and activity-guided engineering of neutrophil membrane-derived therapeutics, including native vesicles and membrane-coated nanomaterials. We further link key engineering parameters-such as membrane orientation, ligand density, glycan architecture, and microdomain integrity-to mechanism-based potency, safety, and translational control. By positioning the neutrophil membrane as a programmable interface rather than a static biomimetic shell, this review outlines a rational roadmap for developing predictable, dose-controlled therapies for infection, inflammatory diseases, and cancer.
SN  - 2211-3835
SN  - 2211-3843
ER  -