Evidence map›Paper›PMID 26891006›Full record

ReviewEuropean journal of immunology2016

Innate lymphoid cells in asthma: Will they take your breath away?

Hye Young Kim, Dale T Umetsu, Rosemarie H Dekruyff

Open access · bronzeAbstract readReview
In one paragraph

Review in European journal of immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
6.1field-weighted citation impact, top 3% 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

41 citing papers in PubMed, 74 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. The RNA-binding protein KSRP reduces asthma-like characteristics in a murine model.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Article
  6. Article
  7. Human keratinocyte response to 4,4'-methylene diphenyl diisocyanate-glutathione conjugate exposure.Xenobiotica; the fate of foreign compounds in biological systems · 2024
    Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Majie Cataplasm Promotes Th1 Response to Fight against Asthmatic Th2 Inflammation through NKs.Evidence-based complementary and alternative medicine : eCAM · 2022
    Article
  15. Review
  16. Article
  17. Interactions between NCRImmune network · 2021
    Article
  18. Review
  19. Review
  20. 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

3 authors at 3 institutions in 3 countries.

Hye Young KimDepartment of Biomedical Sciences, Seoul National University College of Medicine, Seoul, Republic of Korea.
Dale T UmetsuGenentech, One DNA Way, South San Francisco, CA, USA.
Rosemarie H DekruyffDepartment of Medicine, Stanford University, Stanford, CA, USA.
Gene Therapy Laboratory · FRSeoul National University · KRStanford University · US

Funding

TIM recognition of phosphatidylserine regulates innate and adaptive immunityP01AI054456 · NIAID · STANFORD UNIVERSITY · PI FREEMAN, GORDON JAMES · 2003 to 2014
$12.8M
TIM recognition of PtdSer on apoptotic cells and the regulation of immunityR01AI089955 · NIAID · DANA-FARBER CANCER INST · PI DEKRUYFF, ROSEMARIE H, FREEMAN, GORDON JAMES · 2010 to 2014
$2.1M
NIAID NIH HHS P01 AI054456NIAID NIH HHS R01 AI089955
6 · The paper itself

Abstract

Asthma is a complex and heterogeneous disease that is characterized by airway hyper-reactivity (AHR) and airway inflammation. Although asthma was long thought to be driven by allergen-reactive TH 2 cells, it has recently become clear that the pathogenesis of asthma is more complicated and associated with multiple pathways and cell types. A very exciting recent development was the discovery of innate lymphoid cells (ILCs) as key players in the pathogenesis of asthma. ILCs do not express antigen receptors but react promptly to "danger signals" from inflamed tissue and produce an array of cytokines that direct the ensuing immune response. The roles of ILCs may differ in distinct asthma phenotypes. ILC2s may be critical for initiation of adaptive immune responses in inhaled allergen-driven AHR, but may also function independently of adaptive immunity, mediating influenza-induced AHR. ILC2s also contribute to resolution of lung inflammation through their production of amphiregulin. Obesity-induced asthma is associated with expansion of IL-17A-producing ILC3s in the lungs. Furthermore, ILCs may also contribute to steroid-resistant asthma. Although the precise roles of ILCs in different types of asthma are still under investigation, it is clear that inhibition of ILC function represents a potential target that could provide novel treatments for asthma.

Indexed as

Adaptive ImmunityAllergensAmphiregulinAsthmaEGF Family of ProteinsHumansImmunity, InnateInfluenza, HumanInterleukin-17Interleukin-33LungLymphocytesObesitySignal TransductionAllergensAmphiregulinAREG protein, humanEGF Family of ProteinsIL17A protein, humanIL25 protein, humanIL33 protein, humanInterleukin-17Interleukin-33Airway hyper-reactivityAllergyAsthmaInfluenzaInnate lymphoid cellsObesity

Identifiers

PMID26891006
PMCPMC4894653
OpenAlexW2284730656

What OpenQuestion holds

Textmetadata
LicenceTDM
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.