Evidence map›Paper›PMID 37114915›Full record

ArticleRespirology (Carlton, Vic.)2023

Severe asthma ILC2s demonstrate enhanced proliferation that is modified by biologics.

Bilal Malik, Nathan W Bartlett, John W Upham, Kristy S Nichol, John Harrington, Peter A B Wark

Open access · hybridAbstract read
In one paragraph

Article in Respirology (Carlton, Vic.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.9field-weighted citation impact, top 6% of its field
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

21 citing papers in PubMed, 24 citations in OpenAlex.

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  4. Group 2 innate lymphoid cells: Where are we 15 years out?The Journal of allergy and clinical immunology · 2026
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  17. ERJ open research · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 1 country.

Bilal MalikImmune Health Program, Hunter Medical Research Institute, University of Newcastle, Callaghan, New South Wales, Australia.ORCID 0000-0002-9543-7875
Nathan W BartlettImmune Health Program, Hunter Medical Research Institute, University of Newcastle, Callaghan, New South Wales, Australia.
John W UphamDepartment of Respiratory Medicine, Princess Alexandra Hospital, Brisbane, Queensland, Australia.
Kristy S NicholImmune Health Program, Hunter Medical Research Institute, University of Newcastle, Callaghan, New South Wales, Australia.
John HarringtonDepartment of Respiratory and Sleep Medicine, John Hunter Hospital, New Lambton Heights, New South Wales, Australia.ORCID 0000-0003-1542-6250
Peter A B WarkImmune Health Program, Hunter Medical Research Institute, University of Newcastle, Callaghan, New South Wales, Australia.ORCID 0000-0001-5676-6126
Hunter Medical Research Institute · AUJohn Hunter Hospital · AUPrincess Alexandra Hospital · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

objectiveType 2 (T2) innate lymphoid cells (ILC2s) contribute to airway inflammation and disease in asthma. We hypothesize that ILC2s isolated from people with severe allergic and eosinophilic asthma would exhibit an enhanced T2 inflammatory activity that would be altered following treatment with mepolizumab and omalizumab. We compare peripheral blood (PB) isolated ILC2's proliferative capacity, IL-5 and IL-13 secretion and phenotype between healthy without asthma (HC), non-asthma allergic (NAA), mild asthma (MA) and severe allergic and eosinophilic asthma (SA) subjects. We then determined the impact of 6 months treatment with either mepolizumab or omalizumab on ILC2s physiology of SA subjects.

methodsILC2s were sorted and cultured in the presence of IL-2, IL-25, IL-33 and thymic stromal lymphopoietin (TSLP) for 14 days. ILC2s proliferation, phenotypes and functions were assessed using flowcytometry. The ILC2s response was then reassessed following clinically successful treatment of SA subjects with mepolizumab and omalizumab.

resultsSA ILC2s demonstrated increased proliferative capacity, TSLP receptor (TSLPR), GATA3 and NFATc1 protein expressions and increased IL-5 and IL-13 release. ILC2s were also capable of releasing IL-6 in response to stimulation. Mepolizumab treatment reduced ILC2s proliferative capacity and expression of TSLPR, GATA3 and NFATc1. Both mepolizumab and omalizumab were associated with reduced ILC2s release of IL-5 and IL-13, only mepolizumab reduced IL-6.

conclusionILC2s from severe allergic and eosinophilic asthma demonstrated an active phenotype typified by increased proliferation, TSLPR, GATA3 and NFATc1 expression and increased IL-5, IL-13 and IL-6 release. Mepolizumab reduced markers of ILC2s activation.

Indexed as

AsthmaBiological ProductsPulmonary EosinophiliaCell ProliferationCytokinesHumansImmunity, InnateInterleukin-13Interleukin-5Interleukin-6LymphocytesOmalizumabBiological ProductsCytokinesInterleukin-13Interleukin-5Interleukin-6OmalizumabILC2mepolizumabomalizumabproliferationsevere asthmathymic stromal lymphopoietin receptortype 2 cytokinetype 2 innate lymphoid cell

Identifiers

PMID37114915
PMCPMC10946917
OpenAlexW4367312855

What OpenQuestion holds

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LicenceCC BY
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 OpenQuestion graph.