Evidence map›Paper›PMID 27089940›Full record

ArticleImmunology and cell biology2016

Retinoic acid suppresses IL-17 production and pathogenic activity of γδ T cells in CNS autoimmunity.

Mathilde Raverdeau, Conor J Breen, Alicja Misiak, Kingston Hg Mills

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Immunology and cell biology, 2016. 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
3.4field-weighted citation impact, top 8% 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, 38 citations in OpenAlex.

  1. Is Obesity a Modifiable Risk Factor in Multiple Sclerosis? Mechanistic Insights into Neuroinflammation and Oxidative Damage.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026
    Review
  2. Lycopene Supplemented Mediterranean Diet Ameliorates Experimental Autoimmune Encephalomyelitis (EAE) in Mice and Changes Intestinal Microbiome.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025
    Article
  3. The immune system in neurological diseases: What innate-like T cells have to say.The Journal of allergy and clinical immunology · 2024
    Review
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  16. Interleukin (IL)-12 and IL-23 and Their Conflicting Roles in Cancer.Cold Spring Harbor perspectives in biology · 2018
    Review
  17. Review
  18. Review
  19. Taming pathogenic γδ T cells with vitamin A.Immunology and cell biology · 2016
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Mathilde RaverdeauImmune Regulation Research Group, School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin, Ireland.
Conor J BreenDepartment of Biology, Maynooth University, Maynooth, Kildare, Ireland.
Alicja MisiakImmune Regulation Research Group, School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin, Ireland.
Kingston Hg MillsImmune Regulation Research Group, School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin, Ireland.
Trinity College Dublin · IENational University of Ireland, Maynooth · IE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Retinoic acid (RA) in the steady state enhances induction of Foxp3(+) regulatory T (Treg) cells and inhibits differentiation of Th1 and Th17 cells, thereby maintaining tolerance, but can in inflammatory conditions promote effector Th1 and Th17 cells that mediate inflammation. IL-17-producing γδ T cells have recently been shown to have a major pathogenic role in autoimmune diseases. Here, we examined the immunomodulatory effects of RA on γδ T cells. We found that RA had a dramatic suppressive effect on IL-17A and IL-17F production by γδ T cells stimulated with IL-1β and IL-23. RA suppressed RORγt, IL-1R and IL-23R expression in γδ T cells. Treatment of mice with RA suppressed IL-17 production by γδ T cells in vivo. Furthermore, treatment of T cells with RA attenuated their ability to induce disease in experimental autoimmune encephalomyelitis (EAE), a murine model for multiple sclerosis. This was associated with a reduction in the number of central nervous system-infiltrating γδ T cells, but also CD4(+) T cells that produced IL-17A, IL-17F or GM-CSF. Interestingly, treatment of γδ T cells with RA or removal of γδ T cells from a bulk population of T cells significantly reduced their capacity to induce EAE, demonstrating a critical role for γδ T cells in promoting pathogenic Th17 cells. Our findings demonstrate that the anti-inflammatory properties of RA are mediated in part by suppressing STAT3-mediated activation of cytokine production and cytokine receptor expression in γδ T cells, which suppresses their ability to activate Th17 cells.

Indexed as

Adoptive TransferAnimalsAutoimmunityCentral Nervous SystemDisease Models, AnimalEncephalomyelitis, Autoimmune, ExperimentalImmunologic FactorsInterleukin-17Interleukin-1betaInterleukin-23Mice, Inbred C57BLMyelin-Oligodendrocyte GlycoproteinReceptors, Antigen, T-Cell, gamma-deltaTretinoinImmunologic FactorsInterleukin-17Interleukin-1betaInterleukin-23Myelin-Oligodendrocyte GlycoproteinReceptors, Antigen, T-Cell, gamma-deltaTretinoin

Identifiers

PMID27089940
OpenAlexW2342258900

What OpenQuestion holds

Textmetadata
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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.