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Updated: Jan 6, 2026

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Platelets engage mast cells in a bilateral IL-33-driven feed-forward loop.

Airi Nishida1, Jun Nagai1,2,3, Madeline Hastings1

  • 1Division of Allergy and Clinical Immunology, Brigham and Women's Hospital, Boston, MA 02115.

Proceedings of the National Academy of Sciences of the United States of America
|October 9, 2025
PubMed
Summary
This summary is machine-generated.

Platelets and mast cells form a feed-forward loop amplifying type 2 inflammation, particularly in conditions like asthma. This interaction, driven by IL-33, involves platelet activation and mediator release, highlighting a novel innate immune pathway.

Keywords:
IL-33leukotrienesmast cellsnucleotidesplatelets

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A Microphysiological System to Study Leukocyte-Endothelial Cell Interaction during Inflammation
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Area of Science:

  • Immunology
  • Respiratory Medicine
  • Cell Biology

Background:

  • Platelets are known to amplify type 2 inflammation (T2I) via incompletely understood mechanisms.
  • Mast cell (MC) activation in aspirin-exacerbated respiratory disease (AERD) models is dependent on IL-33 and cysteinyl leukotrienes (cysLTs) and is attenuated by platelet depletion.

Purpose of the Study:

  • To elucidate the mechanisms by which platelets amplify T2I, focusing on the interplay between platelets and mast cells.
  • To investigate the role of IL-33 in a potential feed-forward loop involving platelets and mast cells in respiratory inflammation.

Main Methods:

  • Utilized a mouse model of AERD, involving aspirin challenges and analysis of bronchoalveolar lavage (BAL) fluid.
  • Stimulated mouse bone marrow-derived mast cells (BMMCs) with IL-33 and assessed platelet activation markers (CXCL7, CD62P) and mediator production (PGD2, LTC4).
  • Employed genetic deletions of mast cell-specific LTC4 and platelet-specific CysLT2R, and investigated the role of P2Y1 receptors.

Main Results:

  • IL-33 neutralization reduced cysLTs and CXCL7 in BAL fluid from AERD-like mice.
  • BAL fluid PGD2 levels correlated with CXCL7 and MC tryptase in severe asthma patients.
  • Platelets amplified PGD2 and LTC4 production by IL-33-stimulated BMMCs, leading to platelet activation.
  • Genetic deletions of MC-LTC4 or platelet-CysLT2R abrogated platelet activation and mediator amplification.
  • Platelet-derived ADP/ATP and MC P2Y1 receptors were critical for this interplay.

Conclusions:

  • Identified an IL-33-driven feed-forward loop between platelets and mast cells that amplifies T2I.
  • This MC-platelet crosstalk, dependent on cysLTs and P2Y1 receptors, contributes to IL-33-mediated immunopathology in asthma.
  • This pathway represents a potential therapeutic target for T2I-driven respiratory diseases.