Evidence map›Paper›PMID 27111145›Full record

ArticleNature immunology2016

IL-1β, IL-4 and IL-12 control the fate of group 2 innate lymphoid cells in human airway inflammation in the lungs.

Suzanne M Bal, Jochem H Bernink, Maho Nagasawa, Jelle Groot, Medya M Shikhagaie, Kornel Golebski, Cornelis M van Drunen, Rene Lutter, Rene E Jonkers, Pleun Hombrink and 7 more

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In one paragraph

Article in Nature immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 271 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
271citing papers in PubMed, 1 pooled it
27.0field-weighted citation impact, top 1% 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

271 citing papers in PubMed, 1 synthesis or guideline pooled it, 446 citations in OpenAlex.

  1. Pooled it
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  6. Group 2 innate lymphoid cells: Where are we 15 years out?The Journal of allergy and clinical immunology · 2026
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211 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors at 3 institutions in 2 countries.

Suzanne M BalDepartment of Cell Biology and Histology, Academic Medical Center, Amsterdam, the Netherlands.
Jochem H BerninkDepartment of Cell Biology and Histology, Academic Medical Center, Amsterdam, the Netherlands.
Maho NagasawaDepartment of Cell Biology and Histology, Academic Medical Center, Amsterdam, the Netherlands.
Jelle GrootDepartment of Cell Biology and Histology, Academic Medical Center, Amsterdam, the Netherlands.
Medya M ShikhagaieDepartment of Cell Biology and Histology, Academic Medical Center, Amsterdam, the Netherlands.
Kornel GolebskiDepartment of Cell Biology and Histology, Academic Medical Center, Amsterdam, the Netherlands.
Cornelis M van DrunenDepartment of Otorhinolaryngology, Academic Medical Center, Amsterdam, the Netherlands.
Rene LutterDepartment of Experimental Immunology, Academic Medical Center, Amsterdam, the Netherlands.
Rene E JonkersDepartment of Pulmonology, Academic Medical Center, Amsterdam, the Netherlands.
Pleun HombrinkSanquin Research and Landsteiner Laboratory, Amsterdam, the Netherlands.
Melanie BruchardDepartment of Cell Biology and Histology, Academic Medical Center, Amsterdam, the Netherlands.
Julien VillaudyDepartment of Medical Microbiology, Academic Medical Center, Amsterdam, the Netherlands.
J Marius MunnekeDepartment of Hematology, Academic Medical Center, Amsterdam, the Netherlands.
Wytske FokkensDepartment of Otorhinolaryngology, Academic Medical Center, Amsterdam, the Netherlands.
Jonas S ErjefältUnit of Airway Inflammation, Department of Experimental Medical Sciences, Lund University, Lund, Sweden.
Hergen SpitsDepartment of Cell Biology and Histology, Academic Medical Center, Amsterdam, the Netherlands.
Xavier Romero RosDepartment of Cell Biology and Histology, Academic Medical Center, Amsterdam, the Netherlands.
Academic Medical Center · NLLund University · SESanquin · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Group 2 innate lymphoid cells (ILC2s) secrete type 2 cytokines, which protect against parasites but can also contribute to a variety of inflammatory airway diseases. We report here that interleukin 1β (IL-1β) directly activated human ILC2s and that IL-12 induced the conversion of these activated ILC2s into interferon-γ (IFN-γ)-producing ILC1s, which was reversed by IL-4. The plasticity of ILCs was manifested in diseased tissues of patients with severe chronic obstructive pulmonary disease (COPD) or chronic rhinosinusitis with nasal polyps (CRSwNP), which displayed IL-12 or IL-4 signatures and the accumulation of ILC1s or ILC2s, respectively. Eosinophils were a major cellular source of IL-4, which revealed cross-talk between IL-5-producing ILC2s and IL-4-producing eosinophils. We propose that IL-12 and IL-4 govern ILC2 functional identity and that their imbalance results in the perpetuation of type 1 or type 2 inflammation.

Indexed as

Cell PlasticityImmunity, InnateAnimalsCell DifferentiationCells, CulturedEosinophilsFemaleHumansInterferon-gammaInterleukin-12Interleukin-1betaInterleukin-4Lymphocyte ActivationLymphocytesMiceMice, SCIDInterferon-gammaInterleukin-12Interleukin-1betaInterleukin-4

Identifiers

PMID27111145
OpenAlexW2343795401

What OpenQuestion holds

Textmetadata
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.