Evidence map›Paper›PMID 24531377›Full record

ArticleNature medicine2014

FoxA1 directs the lineage and immunosuppressive properties of a novel regulatory T cell population in EAE and MS.

Yawei Liu, Robert Carlsson, Manuel Comabella, Junyang Wang, Michael Kosicki, Belinda Carrion, Maruf Hasan, Xudong Wu, Xavier Montalban, Morten Hanefeld Dziegiel and 4 more

Abstract read
PubMed Publisher
In one paragraph

Article in Nature medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed, 1 pooled it
7.7field-weighted citation impact, top 2% 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

86 citing papers in PubMed, 1 synthesis or guideline pooled it, 154 citations in OpenAlex.

  1. Pooled it
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  14. PRKAG2.2 is essential for FoxA1Science advances · 2023
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26 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 2 institutions in 1 country.

Yawei LiuBiotech Research and Innovation Centre (BRIC), University of Copenhagen, Copenhagen, Denmark.
Robert CarlssonBiotech Research and Innovation Centre (BRIC), University of Copenhagen, Copenhagen, Denmark.
Manuel ComabellaCentre d'Esclerosi Múltiple de Catalunya (CEM-Cat), Unitat de Neuroimmunologia Clínica, Hospital Universitari Vall d´Hebron (HUVH)-Universitat Autònoma de Barcelona, Barcelona, Spain.
Junyang WangBiotech Research and Innovation Centre (BRIC), University of Copenhagen, Copenhagen, Denmark.
Michael KosickiBiotech Research and Innovation Centre (BRIC), University of Copenhagen, Copenhagen, Denmark.
Belinda CarrionBiotech Research and Innovation Centre (BRIC), University of Copenhagen, Copenhagen, Denmark.
Maruf HasanBiotech Research and Innovation Centre (BRIC), University of Copenhagen, Copenhagen, Denmark.
Xudong WuBiotech Research and Innovation Centre (BRIC), University of Copenhagen, Copenhagen, Denmark.
Xavier MontalbanCentre d'Esclerosi Múltiple de Catalunya (CEM-Cat), Unitat de Neuroimmunologia Clínica, Hospital Universitari Vall d´Hebron (HUVH)-Universitat Autònoma de Barcelona, Barcelona, Spain.
Morten Hanefeld DziegielBlood Bank, Copenhagen University Hospital, Copenhagen, Denmark.
Finn SellebjergDanish Multiple Sclerosis Center, University of Copenhagen and Department of Neurology, Rigshospitalet, Copenhagen, Denmark.
Per Soelberg SørensenDanish Multiple Sclerosis Center, University of Copenhagen and Department of Neurology, Rigshospitalet, Copenhagen, Denmark.
Kristian HelinBiotech Research and Innovation Centre (BRIC), University of Copenhagen, Copenhagen, Denmark.
Shohreh Issazadeh-NavikasBiotech Research and Innovation Centre (BRIC), University of Copenhagen, Copenhagen, Denmark.
University of Copenhagen · DKCopenhagen University Hospital · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The defective generation or function of regulatory T (Treg) cells in autoimmune disease contributes to chronic inflammation and tissue injury. We report the identification of FoxA1 as a transcription factor in T cells that, after ectopic expression, confers suppressive properties in a newly identified Treg cell population, herein called FoxA1(+) Treg cells. FoxA1 bound to the Pdl1 promoter, inducing programmed cell death ligand 1 (Pd-l1) expression, which was essential for the FoxA1(+) Treg cells to kill activated T cells. FoxA1(+) Treg cells develop primarily in the central nervous system in response to autoimmune inflammation, have a distinct transcriptional profile and are CD4(+)FoxA1(+)CD47(+)CD69(+)PD-L1(hi)FoxP3(-). Adoptive transfer of stable FoxA1(+) Treg cells inhibited experimental autoimmune encephalomyelitis in a FoxA1-and Pd-l1-dependent manner. The development of FoxA1(+) Treg cells is induced by interferon-β (IFN-β) and requires T cell-intrinsic IFN-α/β receptor (Ifnar) signaling, as the frequency of FoxA1(+) Treg cells was reduced in Ifnb(-/-) and Ifnar(-/-) mice. In individuals with relapsing-remitting multiple sclerosis, clinical response to treatment with IFN-β was associated with an increased frequency of suppressive FoxA1(+) Treg cells in the blood. These findings suggest that FoxA1 is a lineage-specification factor that is induced by IFN-β and supports the differentiation and suppressive function of FoxA1(+) Treg cells.

Indexed as

Gene Expression RegulationAdultAnimalsApoptosisB7-H1 AntigenCell DifferentiationCell LineageCentral Nervous SystemEncephalomyelitis, Autoimmune, ExperimentalFemaleHepatocyte Nuclear Factor 3-alphaHumansImmunosuppression TherapyInterferon-betaMaleMiceB7-H1 AntigenCD274 protein, humanCd274 protein, mouseFOXA1 protein, humanFoxa1 protein, mouseHepatocyte Nuclear Factor 3-alphaInterferon-betaTranscription Factors

Identifiers

PMID24531377
OpenAlexW2052325011

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.