Evidence map›Paper›PMID 26223651›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2015

IL-7/IL-7 Receptor Signaling Differentially Affects Effector CD4+ T Cell Subsets Involved in Experimental Autoimmune Encephalomyelitis.

Carlos A Arbelaez, Simon Glatigny, Rebekka Duhen, Gerard Eberl, Mohamed Oukka, Estelle Bettelli

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 12% 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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.

  1. Association between the IL7R T244I polymorphism and multiple sclerosis risk: a meta analysis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2016
    Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. GM-CSFTheranostics · 2025
    Review
  7. IL-7Rα on CD4Journal of neuroinflammation · 2024
    Article
  8. Article
  9. Observational
  10. Enhanced pathogenicity of Th17 cells due to natalizumab treatment: Implications for MS disease rebound.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. The Association ofNeuropsychiatric disease and treatment · 2022
    Article
  17. Review
  18. Article
  19. Review
  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

6 authors at 3 institutions in 2 countries.

Carlos A ArbelaezDepartment of Immunology, University of Washington, Seattle, WA 98101; Immunology Program, Benaroya Research Institute, Seattle, WA 98101;
Simon GlatignyDepartment of Immunology, University of Washington, Seattle, WA 98101; Immunology Program, Benaroya Research Institute, Seattle, WA 98101;
Rebekka DuhenDepartment of Immunology, University of Washington, Seattle, WA 98101; Immunology Program, Benaroya Research Institute, Seattle, WA 98101;
Gerard EberlLymphoid Tissue Development Unit, Pasteur Institute, Paris 75724, France; and.
Mohamed OukkaDepartment of Immunology, University of Washington, Seattle, WA 98101; Center for Immunity and Immunotherapies, Seattle Children's Research Institute, Seattle, WA 98101.
Estelle BettelliDepartment of Immunology, University of Washington, Seattle, WA 98101; Immunology Program, Benaroya Research Institute, Seattle, WA 98101; ebettelli@benaroyaresearch.org.
Benaroya Research InstituteInstitut Pasteur · FRUniversity of Washington · US

Funding

Molecular mechanisms of Th17 plasticity in MSR01NS081687 · NINDS · BENAROYA RESEARCH INST AT VIRGINIA MASON · PI BETTELLI, ESTELLE, ZIEGLER, STEVEN F · 2013 to 2017
$1.9M
Interplay Between Pathogenic and Regulatory T Cells in EAER01NS059996 · NINDS · BRIGHAM AND WOMEN'S HOSPITAL · PI BETTELLI, ESTELLE · 2008 to 2012
$1.8M
Function of a novel subset of dendritic cells in EAER21NS077116 · NINDS · BENAROYA RESEARCH INST AT VIRGINIA MASON · PI BETTELLI, ESTELLE · 2012 to 2013
$466k
NINDS NIH HHS R01 NS059996NINDS NIH HHS R01 NS081687NINDS NIH HHS R21 NS077116
6 · The paper itself

Abstract

IL-17-producing CD4(+) T (Th17) cells, along with IFN-γ-expressing Th1 cells, represent two major pathogenic T cell subsets in experimental autoimmune encephalomyelitis (EAE), the animal model of multiple sclerosis (MS). The cytokines and transcription factors involved in the development and effector functions of Th1 and Th17 cells have been largely characterized. Among them, IL-23 is essential for the generation of stable and encephalitogenic Th17 cells and for the development of EAE. The IL-7/IL-7R signaling axis participates in cell survival, and perturbation of this pathway has been associated with enhanced susceptibility to MS. A link between IL-23-driven pathogenic T cells and IL-7/IL-7R signaling has previously been proposed, but has not been formally addressed. In the current study, we showed that Th17 cells from mice with EAE express high levels of IL-7Rα compared with Th1 cells. Using mice that constitutively express IL-7Rα on T cells, we determined that sustained IL-7R expression in IL-23R-deficient mice could not drive pathogenic T cells and the development of EAE. IL-7 inhibited the differentiation of Th17 cells, but promoted IFN-γ and GM-CSF secretion in vitro. In vivo IL-7/anti-IL-7 mAb complexes selectively expanded and enhanced the proliferation of CXCR3-expressing Th1 cells, but did not impact Th17 cells and EAE development in wild-type and IL-23R-deficient mice. Importantly, high IL-7 expression was detected in the CNS during EAE and could drive the plasticity of Th17 cells to IFN-γ-producing T cells. Together, these data address the contribution of IL-23/IL-23R and IL-7/IL-7R signaling in Th17 and Th1 cell dynamics during CNS autoimmunity.

Indexed as

AnimalsCD4-Positive T-LymphocytesCell DifferentiationCells, CulturedDisease Models, AnimalEncephalomyelitis, Autoimmune, ExperimentalFlow CytometryHumansInterferon-gammaInterleukin-23Interleukin-7Mice, Inbred C57BLMice, KnockoutMice, TransgenicMultiple SclerosisReceptors, InterleukinInterferon-gammaInterleukin-23interleukin-23 receptor, mouseInterleukin-7Receptors, InterleukinReceptors, Interleukin-7

Identifiers

PMID26223651
PMCPMC4546887
OpenAlexW1862620122

What OpenQuestion holds

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LicenceTDM
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.