Evidence map›Paper›PMID 27827809›Full record

ArticleThe EMBO journal2017

IL-1 signaling is critical for expansion but not generation of autoreactive GM-CSF+ Th17 cells.

Ilgiz A Mufazalov, Carsten Schelmbauer, Tommy Regen, Janina Kuschmann, Florian Wanke, Laureen A Gabriel, Judith Hauptmann, Werner Müller, Emmanuel Pinteaux, Florian C Kurschus and 1 more

Open access · greenAbstract read
In one paragraph

Article in The EMBO journal, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

38 citing papers in PubMed, 56 citations in OpenAlex.

  1. Review
  2. Article
  3. Th17 cell pathogenicity in autoimmune disease.Experimental & molecular medicine · 2025
    Review
  4. Immune-responsive gene 1: The mitochondrial key to Th17 cell pathogenicity in CNS autoimmunity.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. T cells in health and disease.Signal transduction and targeted therapy · 2023
    Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. 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

11 authors at 2 institutions in 2 countries.

Ilgiz A MufazalovInstitute for Molecular Medicine, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany ilgiz.mufazalov@uni-mainz.de waisman@uni-mainz.de.ORCID 0000-0001-9332-0131
Carsten SchelmbauerInstitute for Molecular Medicine, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany.
Tommy RegenInstitute for Molecular Medicine, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany.
Janina KuschmannInstitute for Molecular Medicine, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany.
Florian WankeInstitute for Molecular Medicine, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany.
Laureen A GabrielInstitute for Molecular Medicine, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany.
Judith HauptmannInstitute for Molecular Medicine, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany.
Werner MüllerFaculty of Biology, Medicine and Health, University of Manchester, Manchester, UK.ORCID 0000-0002-1297-9725
Emmanuel PinteauxFaculty of Biology, Medicine and Health, University of Manchester, Manchester, UK.
Florian C KurschusInstitute for Molecular Medicine, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany.
Ari WaismanInstitute for Molecular Medicine, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany ilgiz.mufazalov@uni-mainz.de waisman@uni-mainz.de.ORCID 0000-0003-4304-8234
Johannes Gutenberg University Mainz · DEManchester Academic Health Science Centre · GB

Funding

Medical Research Council G0801296
6 · The paper itself

Abstract

Interleukin-1 (IL-1) is implicated in numerous pathologies, including multiple sclerosis and its animal model experimental autoimmune encephalomyelitis (EAE). However, the exact mechanism by which IL-1 is involved in the generation of pathogenic T cells and in disease development remains largely unknown. We found that following EAE induction, pertussis toxin administration leads to IL-1 receptor type 1 (IL-1R1)-dependent IL-1β expression by myeloid cells in the draining lymph nodes. This myeloid-derived IL-1β did not vitally contribute to the generation and plasticity of Th17 cells, but rather promoted the expansion of a GM-CSF

Indexed as

Cell ProliferationAnimalsEncephalomyelitis, Autoimmune, ExperimentalGranulocyte-Macrophage Colony-Stimulating FactorInterleukin-1MicePertussis ToxinTh17 CellsGranulocyte-Macrophage Colony-Stimulating FactorInterleukin-1Pertussis ToxinautoimmunityEAEGM‐CSFIL‐1Th17

Identifiers

PMID27827809
PMCPMC5210124
OpenAlexW2552240478

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.