Evidence map›Paper›PMID 25689841›Full record

ArticleEuropean journal of immunology2015

NFATc1 deficiency in T cells protects mice from experimental autoimmune encephalomyelitis.

Sarah Reppert, Elisabeth Zinser, Corinna Holzinger, Lena Sandrock, Sonja Koch, Susetta Finotto

Open access · hybridAbstract read
In one paragraph

Article in European journal of immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

23 citing papers in PubMed, 32 citations in OpenAlex.

  1. Trial
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  5. International journal of molecular sciences · 2023
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  10. TACI Constrains TiScience · 2020
    Article
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  17. Loss ofFrontiers in immunology · 2018
    Article
  18. Review
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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

6 authors at 1 institution in 1 country.

Sarah ReppertDepartment of Molecular Pneumology, Friedrich-Alexander-Universität (FAU) Erlangen-Nürnberg, Universitätsklinikum Erlangen, Erlangen, Germany.
Elisabeth ZinserDepartment of Immune Modulation, Friedrich-Alexander-Universität (FAU) Erlangen-Nürnberg, Universitätsklinikum Erlangen, Erlangen, Germany.
Corinna HolzingerDepartment of Molecular Pneumology, Friedrich-Alexander-Universität (FAU) Erlangen-Nürnberg, Universitätsklinikum Erlangen, Erlangen, Germany.
Lena SandrockDepartment of Immune Modulation, Friedrich-Alexander-Universität (FAU) Erlangen-Nürnberg, Universitätsklinikum Erlangen, Erlangen, Germany.
Sonja KochDepartment of Molecular Pneumology, Friedrich-Alexander-Universität (FAU) Erlangen-Nürnberg, Universitätsklinikum Erlangen, Erlangen, Germany.
Susetta FinottoDepartment of Molecular Pneumology, Friedrich-Alexander-Universität (FAU) Erlangen-Nürnberg, Universitätsklinikum Erlangen, Erlangen, Germany.
Universitätsklinikum Erlangen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

NFATc1 is a member of the nuclear factor of activated T cells (NFAT) family of transcription factors. NFAT is activated upon T-cell receptor activation followed by intracytoplasmatic calcium influx where calmodulin, a calcium sensor protein, activates the phosphatase calcineurin that dephosphorylates NFAT proteins and results in NFAT nuclear import. Here, we show the analysis of conditional NFATc1-deficient mice bearing a deletion of NFATc1 in CD4(+) and CD8(+) T cells. NFATc1-deficient CD4(+) T cells polarized under Th17 conditions express reduced levels of the Th17-associated transcription factor RORγT (where ROR is RAR-related orphan receptor) as well as the Th17-associated cytokines IL-17A, IL-17F, IL-21, and IL-10. In the murine model of experimental EAE, we found a strong reduction of the disease outcome in conditional NFATc1-deficient mice, as compared with control littermates. This was accompanied by a diminished inflammation in the brain and spinal cord and reduced IL-17A and IFN-γ expression by antigen-specific spleen, spinal cord, and brain cells. Altogether, these results reveal an important role of NFATc1 in inducing Th17-cell responses and IFN-γ, both being relevant for the EAE development.

Indexed as

AnimalsCell DifferentiationCytokinesDown-RegulationEncephalomyelitis, Autoimmune, ExperimentalInterferon-gammaInterleukin-10Interleukin-17Interleukin-21InterleukinsMiceMice, Inbred C57BLMice, KnockoutNFATC Transcription FactorsNuclear Receptor Subfamily 1, Group F, Member 3Receptors, InterleukinCytokinesIL10 protein, mouseIl17a protein, mouseInterferon-gammaInterleukin-10Interleukin-17Interleukin-21interleukin-23 receptor, mouseInterleukinsNfatc1 protein, mouseNFATC Transcription FactorsNuclear Receptor Subfamily 1, Group F, Member 3Receptors, InterleukinRNA, MessengerRorc protein, mouseTransforming Growth Factor beta1CD4+ T cellsEAENFATRORγTTh17

Identifiers

PMID25689841
PMCPMC6681150
OpenAlexW1574475782

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.