Evidence map›Paper›PMID 24860937›Full record

ArticleCellular immunology2014

γδ T cell subsets play opposing roles in regulating experimental autoimmune encephalomyelitis.

Sarah E Blink, Matthew W Caldis, Gwendolyn E Goings, Christopher T Harp, Bernard Malissen, Immo Prinz, Dan Xu, Stephen D Miller

Open access · greenAbstract read
In one paragraph

Article in Cellular immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

39 citing papers in PubMed, 70 citations in OpenAlex.

  1. 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
  2. Article
  3. Review
  4. Review
  5. The immune system in neurological diseases: What innate-like T cells have to say.The Journal of allergy and clinical immunology · 2024
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. γδ T cells: origin and fate, subsets, diseases and immunotherapy.Signal transduction and targeted therapy · 2023
    Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Frontiers in immunology · 2021
    Article
  17. Article
  18. Article
  19. Article
  20. Review
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

8 authors at 3 institutions in 3 countries.

Sarah E BlinkDepartment of Microbiology-Immunology and Interdepartmental Immunobiology Center, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, United States.
Matthew W CaldisDepartment of Microbiology-Immunology and Interdepartmental Immunobiology Center, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, United States.
Gwendolyn E GoingsDepartment of Microbiology-Immunology and Interdepartmental Immunobiology Center, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, United States.
Christopher T HarpDepartment of Microbiology-Immunology and Interdepartmental Immunobiology Center, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, United States.
Bernard MalissenCentre d'Immunologie de Marseille-Luminy, Université de la Méditerranée, Case 906, Institut National de la Santé et de la Recherche Médicale, U631, Centre National de la Recherche Scientifique, UMR6102, 13288 Marseille, France.
Immo PrinzHannover Medical School, Institute for Immunology, 30625 Hannover, Germany.
Dan XuDepartment of Microbiology-Immunology and Interdepartmental Immunobiology Center, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, United States.
Stephen D MillerDepartment of Microbiology-Immunology and Interdepartmental Immunobiology Center, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, United States. Electronic address: s-d-miller@northwestern.edu.
Northwestern University · USCentre d’Immunologie de Marseille-Luminy · FRMedizinische Hochschule Hannover · DE

Funding

IMMUNOREGULATION AND PATHOLOGY OF CHRONIC-RELAPSING EAER01NS026543 · NINDS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI MILLER, STEPHEN D · 1988 to 2016
$5.0M
NINDS NIH HHS NS-026543NINDS NIH HHS R01 NS026543
6 · The paper itself

Abstract

γδ T cells are resident in cerebrospinal fluid and central nervous system (CNS) lesions of multiple sclerosis (MS) patients, but as multifaceted cells exhibiting innate and adaptive characteristics, their function remains unknown. Previous studies in experimental autoimmune encephalomyelitis (EAE) are contradictory and identified these cells as either promoting or suppressing disease pathogenesis. This study examines distinct γδ T cell subsets during EAE and indicates they mediate differential functions in CNS inflammation and demyelination resulting in pathogenesis or protection. We identified two γδ subsets in the CNS, Vγ1(+) and Vγ4(+), with distinct cytokine profiles and tissue specificity. Anti-γδ T cell receptor (TCR) monoclonal antibody (mAb) administration results in activation and downregulation of surface TCR, rendering the cells undetectable, but with opposing effects: anti-Vγ4 treatment exacerbates disease whereas anti-Vγ1 treatment is protective. The Vγ4(+) subset produces multiple pro-inflammatory cytokines including high levels of IL-17, and accounts for 15-20% of the interleukin-17 (IL-17) producing cells in the CNS, but utilize a variant transcriptional program than CD4(+) Th17 cells. In contrast, the Vγ1 subset produces CCR5 ligands, which may promote regulatory T cell differentiation. γδ T cell subsets thus play distinct and opposing roles during EAE, providing an explanation for previous reports and suggesting selective targeting to optimize regulation as a potential therapy for MS.

Indexed as

AnimalsAntibodies, MonoclonalCell DifferentiationCentral Nervous SystemDown-RegulationEncephalomyelitis, Autoimmune, ExperimentalFemaleInterleukin-17Lymphocyte ActivationMiceMice, Inbred C57BLMice, KnockoutMultiple SclerosisOligodendrogliaReceptors, Antigen, T-Cell, gamma-deltaReceptors, CCR5Antibodies, MonoclonalInterleukin-17Receptors, Antigen, T-Cell, gamma-deltaReceptors, CCR5Adaptive immunityAutoimmunityExperimental autoimmune encephalomyelitisInnate immunityMultiple sclerosisT cellsγδ T cells

Identifiers

PMID24860937
PMCPMC4114040
OpenAlexW2157880544

What OpenQuestion holds

Textmetadata
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.