ArticleAsia Pacific allergy2021
L-type amino acid transporter 1 inhibitor suppresses murine Th2 cell-mediated bronchial hyperresponsiveness independently of eosinophil accumulation.
Article in Asia Pacific allergy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Relationships between basement membrane zone thickness and airway physiology, epithelial gene expression and innate immune cell infiltration in asthma.ERJ open research · 2026Article
- Glutaminolysis of CD4Journal of inflammation research · 2024Review
- Therapeutic Potential for Intractable Asthma by Targeting L-Type Amino Acid Transporter 1.Biomolecules · 2022Review
- Preface of the Proceedings of the 34rd Workshop on Eosinophils in Allergy and Related Diseases 2020 (WEA 2020).Asia Pacific allergy · 2021Article
- Glimpses of the life journey of Prof. Sohei Makino, MD, PhD.Asia Pacific allergy · 2021Article
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe activation of Th2 cells that play a pivotal role in the development of allergic eosinophilic inflammation is regulated by an L-type amino acid transporter (LAT) 1. However, the contribution of LAT1 to the pathogenesis of Th2 cell-mediated airway inflammation has not been investigated.
objectiveIn this study, we investigated the effect of a LAT1 inhibitor, JPH203, on Th2 cell-mediated airway eosinophilic inflammation.
methodsBALB/c mice were transferred with ovalbumin (OVA)-specific Th2 cell and challenged by corresponding allergen with or without administration of JPH203. Then, the infiltration of inflammatory cells including eosinophils and allergen-specific Th2 cells in the lungs and bronchial hyperresponsiveness (BHR) was assessed.
resultsInflammatory responses in the lungs with massive accumulation of eosinophils and BHR were induced in Th2 cell-transferred mice upon challenge with OVA. The treatment with JPH203 significantly suppressed the allergen-induced BHR but not eosinophil infiltration. The infused Th2 cells were also accumulated in the lungs upon allergen challenge, though the response was not affected by JPH203 treatment.
conclusionJPH203 suppressed Th2 cell-mediated BHR through the mechanisms independently of the lung accumulation of eosinophils and Th2 cells.
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