Evidence map›Paper›PMID 27555590›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2016

Protein kinase CK2 governs the molecular decision between encephalitogenic TH17 cell and Treg cell development.

Alexander Ulges, Esther J Witsch, Gautam Pramanik, Matthias Klein, Katharina Birkner, Ulrike Bühler, Beatrice Wasser, Felix Luessi, Natascha Stergiou, Sarah Dietzen and 9 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

29 citing papers in PubMed, 41 citations in OpenAlex.

  1. Review
  2. Article
  3. CK2B Induces CD8Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  4. Article
  5. Drug design, development and therapy · 2025
    Article
  6. Daam2 phosphorylation by CK2α negatively regulates Wnt activity during white matter development and injury.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  7. Article
  8. Review
  9. Protein Kinase CK2 Controls CD8Journal of immunology (Baltimore, Md. : 1950) · 2022
    Article
  10. Review
  11. Review
  12. Protein Kinase CK2 Regulates B Cell Development and Differentiation.Journal of immunology (Baltimore, Md. : 1950) · 2021
    Article
  13. Review
  14. Review
  15. Review
  16. Protein kinase 2 (CK2) controls CD4Mucosal immunology · 2020
    Article
  17. Review
  18. Article
  19. Review
  20. The Balance of Th17 versus Treg Cells in Autoimmunity.International journal of molecular sciences · 2018
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

19 authors at 2 institutions in 1 country.

Alexander UlgesInstitute for Immunology, University Medical Center of the Johannes Gutenberg University of Mainz, 55131 Mainz, Germany;
Esther J WitschDepartment of Neurology, University Medical Center Mainz of the Johannes Gutenberg University of Mainz, 55131 Mainz, Germany;
Gautam PramanikDepartment of Neurology, University Medical Center Mainz of the Johannes Gutenberg University of Mainz, 55131 Mainz, Germany;
Matthias KleinInstitute for Immunology, University Medical Center of the Johannes Gutenberg University of Mainz, 55131 Mainz, Germany;
Katharina BirknerDepartment of Neurology, University Medical Center Mainz of the Johannes Gutenberg University of Mainz, 55131 Mainz, Germany;
Ulrike BühlerDepartment of Neurology, University Medical Center Mainz of the Johannes Gutenberg University of Mainz, 55131 Mainz, Germany;
Beatrice WasserDepartment of Neurology, University Medical Center Mainz of the Johannes Gutenberg University of Mainz, 55131 Mainz, Germany;
Felix LuessiDepartment of Neurology, University Medical Center Mainz of the Johannes Gutenberg University of Mainz, 55131 Mainz, Germany;
Natascha StergiouInstitute for Immunology, University Medical Center of the Johannes Gutenberg University of Mainz, 55131 Mainz, Germany;
Sarah DietzenInstitute for Immunology, University Medical Center of the Johannes Gutenberg University of Mainz, 55131 Mainz, Germany;
Till-Julius BrühlInstitute for Immunology, University Medical Center of the Johannes Gutenberg University of Mainz, 55131 Mainz, Germany;
Toszka BohnInstitute for Immunology, University Medical Center of the Johannes Gutenberg University of Mainz, 55131 Mainz, Germany;
Georg BündgenInstitute for Immunology, University Medical Center of the Johannes Gutenberg University of Mainz, 55131 Mainz, Germany;
Horst KunzInstitute of Organic Chemistry, Johannes Gutenberg University of Mainz, 55128 Mainz, Germany;
Ari WaismanInstitute for Molecular Medicine, University Medical Center of the Johannes Gutenberg University of Mainz, 55131 Mainz, Germany.
Hansjörg SchildInstitute for Immunology, University Medical Center of the Johannes Gutenberg University of Mainz, 55131 Mainz, Germany;
Edgar SchmittInstitute for Immunology, University Medical Center of the Johannes Gutenberg University of Mainz, 55131 Mainz, Germany;
Frauke ZippDepartment of Neurology, University Medical Center Mainz of the Johannes Gutenberg University of Mainz, 55131 Mainz, Germany;
Tobias BoppInstitute for Immunology, University Medical Center of the Johannes Gutenberg University of Mainz, 55131 Mainz, Germany; boppt@uni-mainz.de.
University Medical Center of the Johannes Gutenberg University Mainz · DEJohannes Gutenberg University Mainz · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

T helper 17 (TH17) cells represent a discrete TH cell subset instrumental in the immune response to extracellular bacteria and fungi. However, TH17 cells are considered to be detrimentally involved in autoimmune diseases like multiple sclerosis (MS). In contrast to TH17 cells, regulatory T (Treg) cells were shown to be pivotal in the maintenance of peripheral tolerance. Thus, the balance between Treg cells and TH17 cells determines the severity of a TH17 cell-driven disease and therefore is a promising target for treating autoimmune diseases. However, the molecular mechanisms controlling this balance are still unclear. Here, we report that pharmacological inhibition as well as genetic ablation of the protein kinase CK2 (CK2) ameliorates experimental autoimmune encephalomyelitis (EAE) severity and relapse incidence. Furthermore, CK2 inhibition or genetic ablation prevents TH17 cell development and promotes the generation of Treg cells. Molecularly, inhibition of CK2 leads to reduced STAT3 phosphorylation and strongly attenuated expression of the IL-23 receptor, IL-17, and GM-CSF. Thus, these results identify CK2 as a nodal point in TH17 cell development and suggest this kinase as a potential therapeutic target to treat TH17 cell-driven autoimmune responses.

Indexed as

AnimalsCasein Kinase IIEncephalomyelitis, Autoimmune, ExperimentalForkhead Transcription FactorsGene Expression RegulationGranulocyte-Macrophage Colony-Stimulating FactorHumansInterleukin-17MiceMice, Inbred C57BLMice, TransgenicMultiple SclerosisMyelin-Oligodendrocyte GlycoproteinPeptide FragmentsPhosphorylationReceptors, InterleukinCasein Kinase IIForkhead Transcription FactorsFoxp3 protein, mouseGranulocyte-Macrophage Colony-Stimulating FactorIL23R protein, humanInterleukin-17interleukin-23 receptor, mouseMyelin-Oligodendrocyte Glycoproteinmyelin oligodendrocyte glycoprotein (35-55)Peptide FragmentsReceptors, InterleukinStat3 protein, mouseSTAT3 Transcription FactorFOXP3MS therapymultiple sclerosisregulatory T cellsTH17 cells

Identifiers

PMID27555590
PMCPMC5018788
OpenAlexW2511362679

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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.