Anti-Nectin4 monoclonal antibodies attenuate airway inflammation and epithelial barrier dysfunction in asthma
- 1Department of Internal Medicine, Soonchunhyang University Bucheon Hospital
Abstract
Objective: Nectin4 is an epithelial cell-adhesion molecule that may be involved in airway inflammatory responses. However, the effects of Nectin4 targeting in asthma has not yet been investigated.
Methods: Here we engineered anti-Nectin4 monoclonal antibody, N-1T1C8Ab or N-1T3H9Ab, their effects on airway epithelial dysfunction and inflammation. Dermatophagoides pteronyssinus 1 ( Der p 1)–stimulated normal human bronchial epithelial (NHBE) cells and ovalbumin-induced asthmatic BALB/c mice were used as experimental models.
Results: Anti-Nectin4 antibody treatment restored epithelial barrier dysfunction and was associated with changes in IL-33-related, MyD88/IRAK, and Afadin/Rac1 signaling in NHBE cells. In the murine asthma model, administration of N-1T1C8Ab or N-1T3H9Ab reduced airway inflammation, airway resistance, and immune cell infiltration in bronchoalveolar lavage fluid. Histological analysis demonstrated decreased inflammatory cell infiltration, goblet cell hyperplasia, and fibrosis in lung tissues. Anti-Nectin4 antibody treatment was also associated with modulation of IL-33/MyD88-related signaling components.
Conclusion: These findings indicate that anti-Nectin4 monoclonal antibodies attenuate airway inflammation and improve epithelial barrier function. Further preclinical studies are warranted to determine the potential of Nectin4 targeting in asthma.
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BibTeX
@article{lee2026antinectin4,
title = {{Anti-Nectin4 monoclonal antibodies attenuate airway inflammation and epithelial barrier dysfunction in asthma}},
author = {Pureun-Haneul Lee and MinHyeok An and SangMin Yoon and An-Soo Jang},
journal = {Frontiers in Pharmacology},
year = {2026},
month = oct,
doi = {10.3389/fphar.2026.1931755},
url = {https://www.frontiersin.org/articles/10.3389/fphar.2026.1931755/full},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Anti-Nectin4 monoclonal antibodies attenuate airway inflammation and epithelial barrier dysfunction in asthma
AU - Pureun-Haneul Lee
AU - MinHyeok An
AU - SangMin Yoon
AU - An-Soo Jang
PY - 2026
DA - 2026/10/07
JO - Frontiers in Pharmacology
DO - 10.3389/fphar.2026.1931755
UR - https://www.frontiersin.org/articles/10.3389/fphar.2026.1931755/full
AB - Objective: Nectin4 is an epithelial cell-adhesion molecule that may be involved in airway inflammatory responses. However, the effects of Nectin4 targeting in asthma has not yet been investigated. Methods: Here we engineered anti-Nectin4 monoclonal antibody, N-1T1C8Ab or N-1T3H9Ab, their effects on airway epithelial dysfunction and inflammation. Dermatophagoides pteronyssinus 1 ( Der p 1)–stimulated normal human bronchial epithelial (NHBE) cells and ovalbumin-induced asthmatic BALB/c mice were used as experimental models. Results: Anti-Nectin4 antibody treatment restored epithelial barrier dysfunction and was associated with changes in IL-33-related, MyD88/IRAK, and Afadin/Rac1 signaling in NHBE cells. In the murine asthma model, administration of N-1T1C8Ab or N-1T3H9Ab reduced airway inflammation, airway resistance, and immune cell infiltration in bronchoalveolar lavage fluid. Histological analysis demonstrated decreased inflammatory cell infiltration, goblet cell hyperplasia, and fibrosis in lung tissues. Anti-Nectin4 antibody treatment was also associated with modulation of IL-33/MyD88-related signaling components. Conclusion: These findings indicate that anti-Nectin4 monoclonal antibodies attenuate airway inflammation and improve epithelial barrier function. Further preclinical studies are warranted to determine the potential of Nectin4 targeting in asthma.
SN - 1663-9812
ER -