Uridine diphosphate–glucose/P2Y14R axis is a nonchemokine pathway that selectively promotes eosinophil accumulation
Paul S. Foster,1 Hock L. Tay,1 and Simon P. Hogan2
1School of Biomedical Sciences and Pharmacy, Faculty of Health and Medicine, University of Newcastle, and Hunter Medical Research Institute (HMRI), Newcastle, New South Wales, Australia.
2Mary H. Weiser Food Allergy Center, Department of Pathology, Michigan Medicine, University of Michigan, Ann Arbor, Michigan, USA.
Address correspondence to: Simon P. Hogan, Michigan Medicine, University of Michigan, 4051-BSRB, 109 Zina Pitcher Place, Ann Arbor, Michigan 48109-2200, USA. Phone:734.647.9923; Email: sihogan@med.umich.edu.
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1School of Biomedical Sciences and Pharmacy, Faculty of Health and Medicine, University of Newcastle, and Hunter Medical Research Institute (HMRI), Newcastle, New South Wales, Australia.
2Mary H. Weiser Food Allergy Center, Department of Pathology, Michigan Medicine, University of Michigan, Ann Arbor, Michigan, USA.
Address correspondence to: Simon P. Hogan, Michigan Medicine, University of Michigan, 4051-BSRB, 109 Zina Pitcher Place, Ann Arbor, Michigan 48109-2200, USA. Phone:734.647.9923; Email: sihogan@med.umich.edu.
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1School of Biomedical Sciences and Pharmacy, Faculty of Health and Medicine, University of Newcastle, and Hunter Medical Research Institute (HMRI), Newcastle, New South Wales, Australia.
2Mary H. Weiser Food Allergy Center, Department of Pathology, Michigan Medicine, University of Michigan, Ann Arbor, Michigan, USA.
Address correspondence to: Simon P. Hogan, Michigan Medicine, University of Michigan, 4051-BSRB, 109 Zina Pitcher Place, Ann Arbor, Michigan 48109-2200, USA. Phone:734.647.9923; Email: sihogan@med.umich.edu.
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Hogan, S.
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Published April 1, 2021 - More info
J Clin Invest. 2021;131(7):e147735. https://doi.org/10.1172/JCI147735.
© 2021 American Society for Clinical Investigation
Allergic asthma is a chronic inflammatory airway disease characterized by dysregulated type 2 immune responses, including degranulating airway eosinophils that induce tissue damage and airway hyperresponsiveness (AHR). The type 2 cytokines interleukin 5 (IL-5) and IL-13 and the eosinophil-specific chemokine CCL11/CCL24/CCL26 axis recruit, activate, and regulate eosinophils in the airways. In this issue of the JCI, Karcz et al. identified a mechanism involving the nucleotide sugar UDP-glucose (UDP-G) and the purinergic receptor P2Y14R in amplifying eosinophil accumulation in the lung. During type 2 inflammation, UDP-G activates P2Y14R on eosinophils, inducing the cells to move and migrate into the lung. Pharmacologically or genetically inhibiting P2Y14R on eosinophils attenuated eosinophil infiltration and AHR. Future experiments, including identifying additional type 2 factors regulating P2Y14R expression on lung eosinophils, are necessary to ascertain the impact of targeting P2Y14R as an alternative or adjunctive therapy to current type 2 biologics for the treatment of asthma.
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