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REVIEW article

Front. Allergy

Sec. Mechanisms in Allergy

Volume 6 - 2025 | doi: 10.3389/falgy.2025.1585142

This article is part of the Research Topic Update on Eosinophil-associated diseases View all 3 articles

Regulation of eosinophil recruitment and heterogeneity during allergic airway inflammation

Provisionally accepted
  • University Hospital, Department of Infection Biology, University of Erlangen Nuremberg, Erlangen, Germany

The final, formatted version of the article will be published soon.

    Eosinophils represent a granulocyte cell type that is strongly associated with type 2 inflammatory conditions. During steady state conditions few eosinophils are found in lung tissue, though they may contribute to homeostasis. In allergic airway inflammation, eosinophils are strongly increased and associated to disease severity. The underlying type 2 immune response tightly regulates eosinophil development, recruitment, survival, and heterogeneity.Inflammatory eosinophils in the lung are unfavourable, as they can cause tissue damage, amplify type 2 immunity and induce bronchial obstruction by expelling granular proteins and cytokines. In this review we provide an overview about mechanisms regulating development of eosinophils in the bone marrow and their extravasation into the lung including recent findings on induction and diversity of eosinophilia in allergic airway inflammation.

    Keywords: Eosinophils, Allergic Airway Inflammation, Type 2 immunity, Asthma, IL-5

    Received: 28 Feb 2025; Accepted: 31 Mar 2025.

    Copyright: © 2025 Graf, Radtke and Voehringer. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence: David Voehringer, University Hospital, Department of Infection Biology, University of Erlangen Nuremberg, Erlangen, 91054, Germany

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.

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