Evidence mapPaperPMID 39855362Full record

ReviewThe Journal of allergy and clinical immunology2025

Targeting alarmins in asthma: From bench to clinic.

Ayobami Akenroye, Joshua A Boyce, Hirohito Kita

Abstract readReview
In one paragraph

Review in The Journal of allergy and clinical immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

30 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Vascular remodeling in asthma: from mechanisms to precision medicine.Current opinion in allergy and clinical immunology · 2026
    Review
  3. Group 2 innate lymphoid cells: Where are we 15 years out?The Journal of allergy and clinical immunology · 2026
    Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Emerging Systemic Treatments for Asthma and Allergic Diseases: New Tricks, Same Dog?The journal of allergy and clinical immunology. In practice · 2026
    Review
  17. Review
  18. Article
  19. Review
  20. Frontiers in medicine · 2026
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Ayobami AkenroyeJeff and Penny Vinik Immunology Center, Division of Allergy and Clinical Immunology, Brigham and Women's Hospital, Boston, Mass; Channing Division of Network Medicine, Brigham and Women's Hospital, Boston, Mass; Department of Medicine, Harvard Medical School, Boston, Mass. Electronic address: aakenroye@bwh.harvard.edu.
Joshua A BoyceJeff and Penny Vinik Immunology Center, Division of Allergy and Clinical Immunology, Brigham and Women's Hospital, Boston, Mass; Department of Medicine, Harvard Medical School, Boston, Mass.
Hirohito KitaDivision of Allergy, Asthma and Clinical Immunology, the Department of Medicine, and the Department of Immunology, Mayo Clinic Arizona, Scottsdale, Ariz; Department of Immunology, Mayo Clinic Rochester, Rochester, Minn.

Funding

Mechanisms of Allergen-induced Type 2 ImmunityR37AI071106 · NIAID · MAYO CLINIC ARIZONA · 2023 to 2025
$1.2M
Mechanisms of IL-33 secretion in allergic diseasesR01AI128729 · NIAID · MAYO CLINIC ARIZONA · 2021 to 2025
$1.1M
NIAID NIH HHS R01 AI128729NIAID NIH HHS R37 AI071106
6 · The paper itself

Abstract

Over the past 2 decades, mechanistic studies of allergic and type 2 (T2)-mediated airway inflammation have led to multiple approved therapies for the treatment of moderate-to-severe asthma. The approval and availability of these monoclonal antibodies targeting IgE, a T2 cytokine (IL-5) and/or cytokine receptors (IL-5Rα, IL-4Rα) has been central to the progresses made in the management of moderate-to-severe asthma over this period. However, there are persistent gaps in clinician's ability to provide precise care, given that many patients with T2-high asthma do not respond to IgE- or T2 cytokine-targeting therapies and that patients with T2-low asthma have few therapeutic options. The new frontier of precision medicine in asthma, as well as in other allergic diseases, includes the targeting of epithelium-derived cytokines known as alarmins, including thymic stromal lymphopoietin, IL-25, IL-33, and their receptors. The effects of these alarmins, which can act upstream of immune cells, involve both the innate and adaptive systems and hold potential for the treatment of both T2-high and -low disease. Tezepelumab, an anti-thymic stromal lymphopoietin antibody, has already been approved for the treatment of severe asthma. In this review, we discuss our current understanding of alarmin biology with a primary focus on allergic airway diseases. We link the mechanistic corollaries to the clinical implications and advances in drug development targeting alarmins, with a particular focus on currently approved treatments, those under study, and future potential targets in alarmin signaling pathways.

Indexed as

AlarminsAnti-Asthmatic AgentsAsthmaAnimalsAntibodies, MonoclonalCytokinesHumansAlarminsAnti-Asthmatic AgentsAntibodies, MonoclonalCytokinesairway inflammationAlarminsallergic airway diseaseastegolimabbasophilsdendritic cellseosinophilsepithelial derived cytokinesetokimabIL-17RAIL-17RBIL-25IL-33ILRL1itepekimabmast cellsOX40LST2tezepelumabTLR4TSLPTSLPRtuft cells

Identifiers

PMID39855362
PMCPMC12555011

What Socratic holds

Textmetadata
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Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.