Evidence map›Paper›PMID 31852728›Full record

ArticleImmunoHorizons2019

Development of Type 2 Innate Lymphoid Cells Is Selectively Inhibited by Sustained E Protein Activity.

Hannah Berrett, Liangyue Qian, Olga Roman, Alanis Cordova, Amie Simmons, Xiao-Hong Sun, José Alberola-Ila

Open access · goldAbstract read
In one paragraph

Article in ImmunoHorizons, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.3field-weighted citation impact, top 39% 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

5 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. ILC Differentiation in the Thymus.Advances in experimental medicine and biology · 2022
    Article
  5. 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

7 authors at 1 institution in 1 country.

Hannah BerrettArthritis and Clinical Immunology Program, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104; and.
Liangyue QianArthritis and Clinical Immunology Program, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104; and.ORCID 0000-0003-0265-1985
Olga RomanArthritis and Clinical Immunology Program, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104; and.
Alanis CordovaArthritis and Clinical Immunology Program, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104; and.
Amie SimmonsArthritis and Clinical Immunology Program, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104; and.
Xiao-Hong SunArthritis and Clinical Immunology Program, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104; and.ORCID 0000-0002-7390-7506
José Alberola-IlaArthritis and Clinical Immunology Program, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104; and alberolaj@omrf.org.ORCID 0000-0003-2439-553X
Oklahoma Medical Research Foundation · US

Funding

Characterization of a distinct NKT subset and its role in influenza responsesR01AI129458 · NIAID · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI ALBEROLA-ILA, JOSE · 2018 to 2022
$2.7M
Exploring the thymic origin of group 2 innate lymphoid cellsR01AI126851 · NIAID · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI SUN, XIAO-HONG · 2016 to 2020
$2.7M
E protein activity regulates effector lineage differentiation of NKT and ILCsR21AI122693 · NIAID · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI ALBEROLA-ILA, JOSE · 2016 to 2017
$472k
NIAID NIH HHS R01 AI126851NIAID NIH HHS R01 AI129458NIAID NIH HHS R21 AI122693
6 · The paper itself

Abstract

Innate lymphoid cells (ILCs) are tissue-resident lymphoid cells that reside mostly at barrier surfaces and participate in the initial response against pathogens. They are classified into different types based on effector programs that are based on cytokine production and transcription factor expression. They all derive from the common lymphoid precursor, but the molecular mechanisms regulating ILC subset development is not well understood. Experiments using Id2 knockout mice have previously shown that E protein activity inhibition is an absolute requirement for the development of all ILC subsets. In this study, we use a genetic approach to demonstrate that small increases in E protein activity during ILC development selectively inhibit type 2 ILC development. Type 1 ILCs are mostly unperturbed, and type 3 ILC show only a minor inhibition. This effect is first evident at the ILC2 progenitor stage and is ILC intrinsic. Therefore, our results demonstrate that modulation of E protein activity can bias cell fate decisions in developing ILCs.

Indexed as

AnimalsBasic Helix-Loop-Helix ProteinsCell Cycle ProteinsCell DifferentiationFemaleGene Expression RegulationGene Knock-In TechniquesImmunity, InnateLymphoid Progenitor CellsMaleMiceMice, TransgenicNatural Killer T-CellsTranscription Factor 4Basic Helix-Loop-Helix ProteinsCell Cycle ProteinsCep63 protein, mouseTcf12 protein, mouseTcf3 protein, mouseTcf4 protein, mouseTranscription Factor 4

Identifiers

PMID31852728
PMCPMC6938226
OpenAlexW2995070484

What OpenQuestion 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 OpenQuestion graph.