Evidence map›Paper›PMID 28099418›Full record

ArticleNature2017

IL-17 is a neuromodulator of Caenorhabditis elegans sensory responses.

Changchun Chen, Eisuke Itakura, Geoffrey M Nelson, Ming Sheng, Patrick Laurent, Lorenz A Fenk, Rebecca A Butcher, Ramanujan S Hegde, Mario de Bono

Open access · greenAbstract read
In one paragraph

Article in Nature, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed
6.1field-weighted citation impact, top 3% 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

76 citing papers in PubMed, 133 citations in OpenAlex.

  1. The neuroimmune system and cognition.Nature immunology · 2026
    Review
  2. Article
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  7. M cell-dependent commensal uptake confers encephalitogenic phenotypes on γδT17 cells in Peyer's patches.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  8. Maladaptive immunity to the microbiota promotes neuronal hyperinnervation and itch via IL-17A.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Brain interleukins and Alzheimer's disease.Metabolic brain disease · 2025
    Review
  16. Review
  17. Review
  18. The many roads toJournal of biosciences · 2025
    Review
  19. Article
  20. Article

16 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 2 countries.

Changchun ChenMRC Laboratory of Molecular Biology, Francis Crick Avenue, Cambridge CB2 0QH, UK.
Eisuke ItakuraMRC Laboratory of Molecular Biology, Francis Crick Avenue, Cambridge CB2 0QH, UK.
Geoffrey M NelsonMRC Laboratory of Molecular Biology, Francis Crick Avenue, Cambridge CB2 0QH, UK.
Ming ShengMRC Laboratory of Molecular Biology, Francis Crick Avenue, Cambridge CB2 0QH, UK.
Patrick LaurentMRC Laboratory of Molecular Biology, Francis Crick Avenue, Cambridge CB2 0QH, UK.
Lorenz A FenkMRC Laboratory of Molecular Biology, Francis Crick Avenue, Cambridge CB2 0QH, UK.
Rebecca A ButcherDepartment of Chemistry, University of Florida, Gainesville, Florida 32611, USA.
Ramanujan S HegdeMRC Laboratory of Molecular Biology, Francis Crick Avenue, Cambridge CB2 0QH, UK.
Mario de BonoMRC Laboratory of Molecular Biology, Francis Crick Avenue, Cambridge CB2 0QH, UK.
MRC Laboratory of Molecular Biology · GBUniversity of Florida · US

Funding

Enhancing and expanding the CGC Strain CollectionP40OD010440 · OD · UNIVERSITY OF MINNESOTA · PI Ann E. Rougvie · 2012 to 2026
$7.5M
European Research Council 269058Medical Research Council MC_U105178786Medical Research Council MC_UP_A022_1007NIH HHS P40 OD010440
6 · The paper itself

Abstract

Interleukin-17 (IL-17) is a major pro-inflammatory cytokine: it mediates responses to pathogens or tissue damage, and drives autoimmune diseases. Little is known about its role in the nervous system. Here we show that IL-17 has neuromodulator-like properties in Caenorhabditis elegans. IL-17 can act directly on neurons to alter their response properties and contribution to behaviour. Using unbiased genetic screens, we delineate an IL-17 signalling pathway and show that it acts in the RMG hub interneurons. Disrupting IL-17 signalling reduces RMG responsiveness to input from oxygen sensors, and renders sustained escape from 21% oxygen transient and contingent on additional stimuli. Over-activating IL-17 receptors abnormally heightens responses to 21% oxygen in RMG neurons and whole animals. IL-17 deficiency can be bypassed by optogenetic stimulation of RMG. Inducing IL-17 expression in adults can rescue mutant defects within 6 h. These findings reveal a non-immunological role of IL-17 modulating circuit function and behaviour.

Indexed as

AnimalsBehavior, AnimalCaenorhabditis elegansCaenorhabditis elegans ProteinsHEK293 CellsHumansInterleukin-17InterneuronsOxygenReceptors, Interleukin-17SensationSignal TransductionACTL-1 protein, C elegansCaenorhabditis elegans ProteinsInterleukin-17NFKI-1 protein, C elegansOxygenReceptors, Interleukin-17

Identifiers

PMID28099418
PMCPMC5503128
OpenAlexW2576526246

What OpenQuestion holds

Textmetadata
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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.