Evidence map›Paper›PMID 31509749›Full record

ArticleCell reports2019

Orphan Nuclear Receptor NR2F6 Suppresses T Follicular Helper Cell Accumulation through Regulation of IL-21.

William J Olson, Bojana Jakic, Verena Labi, Katia Schoeler, Michaela Kind, Victoria Klepsch, Gottfried Baier, Natascha Hermann-Kleiter

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

19 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
  2. Article
  3. Loss of NR2F6 Protects from Salmonella Typhimurium Infection.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
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  6. Review
  7. Article
  8. Article
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  13. Review
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  16. Article
  17. NR2F6 as a Prognostic Biomarker in HNSCC.International journal of molecular sciences · 2020
    Article
  18. Review
  19. Article
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

8 authors at 2 institutions in 1 country.

William J OlsonInstitute of Cell Genetics, Department for Genetics and Pharmacology, Medical University of Innsbruck, Peter Mayr Str. 1a, 6020 Innsbruck, Austria.
Bojana JakicInstitute of Cell Genetics, Department for Genetics and Pharmacology, Medical University of Innsbruck, Peter Mayr Str. 1a, 6020 Innsbruck, Austria.
Verena LabiDivision of Developmental Immunology, Biocenter, Medical University of Innsbruck, Innsbruck, Innrain 80, 6020 Innsbruck, Austria.
Katia SchoelerDivision of Developmental Immunology, Biocenter, Medical University of Innsbruck, Innsbruck, Innrain 80, 6020 Innsbruck, Austria.
Michaela KindInstitute of Cell Genetics, Department for Genetics and Pharmacology, Medical University of Innsbruck, Peter Mayr Str. 1a, 6020 Innsbruck, Austria.
Victoria KlepschInstitute of Cell Genetics, Department for Genetics and Pharmacology, Medical University of Innsbruck, Peter Mayr Str. 1a, 6020 Innsbruck, Austria.
Gottfried BaierInstitute of Cell Genetics, Department for Genetics and Pharmacology, Medical University of Innsbruck, Peter Mayr Str. 1a, 6020 Innsbruck, Austria.
Natascha Hermann-KleiterInstitute of Cell Genetics, Department for Genetics and Pharmacology, Medical University of Innsbruck, Peter Mayr Str. 1a, 6020 Innsbruck, Austria. Electronic address: natascha.kleiter@i-med.ac.at.
Universität Innsbruck · ATInnsbruck Medical University · AT

Funding

Austrian Science Fund FWF P 28694Austrian Science Fund FWF P 30324Austrian Science Fund FWF P 31383Austrian Science Fund FWF W 1101European Research Council 786462
6 · The paper itself

Abstract

CD4 T follicular helper (Tfh) cells are specialized in helping B cells during the germinal center (GC) reaction and ultimately promote long-term humoral immunity. Here we report that loss of the nuclear orphan receptor NR2F6 causes enhanced survival and accumulation of Tfh cells, GC B cells, and plasma cells (PCs) following T cell-dependent immunization. Nr2f6-deficient CD4 T cell dysfunction is the primary cause of cell accumulation. Cytokine expression in Nr2f6-deficient Tfh cells is dysregulated, and Il21 expression is enhanced. Mechanistically, NR2F6 binds directly to the interleukin 21 (IL-21) promoter and a conserved noncoding sequence (CNS) near the Il21 gene in resting CD4

Indexed as

Adoptive TransferAnimalsB-LymphocytesCD4-Positive T-LymphocytesCell DifferentiationCells, CulturedChromatin ImmunoprecipitationGerminal CenterInterleukin-21InterleukinsLymphocyte ActivationMiceMice, Inbred C57BLMice, KnockoutOrphan Nuclear ReceptorsPlasma CellsInterleukin-21InterleukinsNr2f6 protein, mouseOrphan Nuclear ReceptorsReceptors, Interleukin-21Repressor Proteinsautoimmunitygerminal center reactionIL-21immunizationnuclear receptorsystemic lupus erythematosusT follicular helper cell

Identifiers

PMID31509749
PMCPMC6791812
OpenAlexW2947460681

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.