Evidence map›Paper›PMID 41577142›Full record

ArticleThe Journal of allergy and clinical immunology2026

Platelet-macrophage cooperation drives IL-33-dependent type 2 lung immunopathology in a sex-biased manner.

Hiroaki Hayashi, Jun Nagai, Juying Lai, Kendall Zaleski, Chunli Feng, Madeline Hastings, Airi Nishida, Yumi Tani, Junrui Lin, Marie Sasaki and 5 more

Abstract read
In one paragraph

Article in The Journal of allergy and clinical immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–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

1 citing paper in PubMed.

  1. 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

15 authors.

Hiroaki HayashiDivision of Allergy and Clinical Immunology, Brigham and Women's Hospital, Boston, Mass; Jeff and Penny Vinik Center for Allergic Disease Research, Boston, Mass; Department of Medicine, Harvard Medical School, Boston, Mass.
Jun NagaiDivision of Allergy and Clinical Immunology, Brigham and Women's Hospital, Boston, Mass; Jeff and Penny Vinik Center for Allergic Disease Research, Boston, Mass; Department of Medicine, Harvard Medical School, Boston, Mass.
Juying LaiDivision of Allergy and Clinical Immunology, Brigham and Women's Hospital, Boston, Mass; Jeff and Penny Vinik Center for Allergic Disease Research, Boston, Mass.
Kendall ZaleskiDivision of Allergy and Clinical Immunology, Brigham and Women's Hospital, Boston, Mass; Jeff and Penny Vinik Center for Allergic Disease Research, Boston, Mass.
Chunli FengDivision of Allergy and Clinical Immunology, Brigham and Women's Hospital, Boston, Mass; Jeff and Penny Vinik Center for Allergic Disease Research, Boston, Mass.
Madeline HastingsDivision of Allergy and Clinical Immunology, Brigham and Women's Hospital, Boston, Mass; Jeff and Penny Vinik Center for Allergic Disease Research, Boston, Mass.
Airi NishidaDivision of Allergy and Clinical Immunology, Brigham and Women's Hospital, Boston, Mass; Jeff and Penny Vinik Center for Allergic Disease Research, Boston, Mass.
Yumi TaniDivision of Allergy and Clinical Immunology, Brigham and Women's Hospital, Boston, Mass; Jeff and Penny Vinik Center for Allergic Disease Research, Boston, Mass.
Junrui LinDivision of Allergy and Clinical Immunology, Brigham and Women's Hospital, Boston, Mass; Jeff and Penny Vinik Center for Allergic Disease Research, Boston, Mass.
Marie SasakiDivision of Allergy and Clinical Immunology, Brigham and Women's Hospital, Boston, Mass; Jeff and Penny Vinik Center for Allergic Disease Research, Boston, Mass.
Kinan AlhallakDivision of Allergy and Clinical Immunology, Brigham and Women's Hospital, Boston, Mass; Jeff and Penny Vinik Center for Allergic Disease Research, Boston, Mass.
Sofia A MarshallDivision of Allergy and Clinical Immunology, Brigham and Women's Hospital, Boston, Mass; Jeff and Penny Vinik Center for Allergic Disease Research, Boston, Mass.
Tao LiuDivision of Allergy and Clinical Immunology, Brigham and Women's Hospital, Boston, Mass; Jeff and Penny Vinik Center for Allergic Disease Research, Boston, Mass; Department of Medicine, Harvard Medical School, Boston, Mass.
Barbara BalestrieriDivision of Allergy and Clinical Immunology, Brigham and Women's Hospital, Boston, Mass; Jeff and Penny Vinik Center for Allergic Disease Research, Boston, Mass; Department of Medicine, Harvard Medical School, Boston, Mass.
Joshua A BoyceDivision of Allergy and Clinical Immunology, Brigham and Women's Hospital, Boston, Mass; Jeff and Penny Vinik Center for Allergic Disease Research, Boston, Mass; Department of Medicine, Harvard Medical School, Boston, Mass. Electronic address: jboyce@bwh.harvard.edu.

Funding

Therapeutic Control of Aspirin-Exacerbated Respiratory DiseaseU19AI095219 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI Tanya Maria Laidlaw · 2011 to 2026
$29.1M
Regulation of Pulmonary Prostaglandins by Leukotriene E4R01AI078908 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI BOYCE, JOSHUA A · 2009 to 2025
$8.8M
Eicosanoid Networks in Aspirin HypersensitivityR01AI136041 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI Joshua A Boyce · 2018 to 2026
$5.4M
CysLT and P2Y Receptors in Lung InflammationR37AI052353 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI BOYCE, JOSHUA A · 2013 to 2022
$5.2M
Prostaglandin E2-Dependent Control of a Mast Cell IL-33/ST2 Pathway in AsthmaR01AI175149 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI Joshua A Boyce · 2023 to 2026
$3.4M
Eicosanoid Networks in Aspirin Exacerbated Respiratory DiseaseR01HL117945 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI BOYCE, JOSHUA A · 2013 to 2016
$1.5M
The inflammatory role of the platelet in aspirin-exacerbated respiratory disease.K23HL111113 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI LAIDLAW, TANYA MARIA · 2012 to 2016
$721k
NHLBI NIH HHS K23 HL111113NHLBI NIH HHS R01 HL117945NIAID NIH HHS R01 AI078908NIAID NIH HHS R01 AI136041NIAID NIH HHS R01 AI175149NIAID NIH HHS R37 AI052353NIAID NIH HHS U19 AI095219
6 · The paper itself

Abstract

backgroundPlatelets amplify lung type 2 inflammation (T2I), but the underlying mechanisms remain incompletely understood.

objectiveWe elucidated the platelet-driven T2I mechanisms, particularly the role of platelet-derived leukotriene C

methodsWe assessed lung T2I to Alternaria alternata extract in vivo using mice with targeted deletions of Ltc4s in platelets, macrophages (Macs), or mast cells (MCs); Il33 in Macs, hematopoietic cells, or alveolar type 2 (AT2) cells; and cysteinyl leukotriene receptors. Exogenous administration of LTC

resultsPlatelets promoted IL-33 expression in perivascular Macs and induced transcellular LTC

conclusionAdherent platelets rapidly upregulate IL-33-expressing Macs, and platelet-derived LTC

Indexed as

Blood PlateletsInterleukin-33LungMacrophagesPneumoniaAlternariaAnimalsFemaleLeukotriene C4MaleMiceMice, Inbred C57BLMice, KnockoutSex FactorsIl33 protein, mouseInterleukin-33Leukotriene C4alveolar type 2 cellgroup 2 innate lymphoid cellIL-33leukotrienemacrophagePlatelet

Identifiers

PMID41577142
PMCPMC13003346

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.