Evidence map›Paper›PMID 38540714›Full record

ReviewBiomolecules2024

TNF Superfamily and ILC2 Activation in Asthma.

Takahiro Matsuyama, Brittany Marie Salter, Nahal Emami Fard, Kentaro Machida, Roma Sehmi

Open access · goldAbstract readReview
In one paragraph

Review in Biomolecules, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

9 citing papers in PubMed, 8 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Metabolic Reprogramming and ILC2 Plasticity in Obesity-related Asthma.Clinical reviews in allergy & immunology · 2026
    Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
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

5 authors at 2 institutions in 2 countries.

Takahiro MatsuyamaRespiratory Research Group, Department of Medicine, McMaster University, Hamilton, ON L8S 4L8, Canada.ORCID 0009-0009-5167-8579
Brittany Marie SalterRespiratory Research Group, Department of Medicine, McMaster University, Hamilton, ON L8S 4L8, Canada.
Nahal Emami FardRespiratory Research Group, Department of Medicine, McMaster University, Hamilton, ON L8S 4L8, Canada.
Kentaro MachidaDepartment of Pulmonary Medicine, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima 890-8520, Japan.ORCID 0000-0002-9394-091X
Roma SehmiRespiratory Research Group, Department of Medicine, McMaster University, Hamilton, ON L8S 4L8, Canada.ORCID 0000-0003-0968-6304
McMaster University · CAKagoshima University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Eosinophilic asthma is the most prevalent and well-defined phenotype of asthma. Despite a majority of patients responding to corticosteroid therapy and T2 biologics, there remains a subset that have recurrent asthma exacerbations, highlighting a need for additional therapies to fully ameliorate airway eosinophilia. Group 2 innate lymphoid cells (ILC2) are considered key players in the pathogenesis of eosinophilic asthma through the production of copious amounts of type 2 cytokines, namely IL-5 and IL-13. ILC2 numbers are increased in the airways of asthmatics and with the greatest numbers of activated ILC2 detected in sputa from severe prednisone-dependent asthma with uncontrolled eosinophilia. Although epithelial-derived cytokines are important mediators of ILC2 activation, emerging evidence suggests that additional pathways stimulate ILC2 function. The tumor necrosis factor super family (TNFSF) and its receptors (TNFRSF) promote ILC2 activity. In this review, we discuss evidence supporting a relationship between ILC2 and TNFSF/TNFRSF axis in eosinophilic asthma and the role of this relationship in severe asthma with airway autoimmune responses.

Indexed as

AsthmaPulmonary EosinophiliaCytokinesHumansImmunity, InnateLymphocytesCytokinesairway autoimmune responseeosinophilic asthmaGITRLgroup 2 innate lymphoid cellOX40LRANKLTL1ATNFTNFSF

Identifiers

PMID38540714
PMCPMC10967788
OpenAlexW4392296563

What OpenQuestion holds

Textmetadata
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.