Evidence map›Paper›PMID 30226829›Full record

ArticleThe Journal of clinical investigation2018

CNS-resident classical DCs play a critical role in CNS autoimmune disease.

David A Giles, Patrick C Duncker, Nicole M Wilkinson, Jesse M Washnock-Schmid, Benjamin M Segal

Open access · greenAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

59 citing papers in PubMed, 105 citations in OpenAlex.

  1. Paradoxical Expression of Ionotropic Glutamate Receptors in Leucocytes.Clinical reviews in allergy & immunology · 2026
    Article
  2. Article
  3. Frontiers in cellular neuroscience · 2026
    Review
  4. Review
  5. Article
  6. An IL-23-STAT4 pathway is required for the proinflammatory function of classical dendritic cells during CNS inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  7. Article
  8. CNS Resident Innate Immune Cells: Guardians of CNS Homeostasis.International journal of molecular sciences · 2024
    Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
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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

5 authors at 3 institutions in 2 countries.

David A GilesHoltom-Garrett Program in Neuroimmunology, Department of Neurology.
Patrick C DunckerHoltom-Garrett Program in Neuroimmunology, Department of Neurology.
Nicole M WilkinsonHoltom-Garrett Program in Neuroimmunology, Department of Neurology.
Jesse M Washnock-SchmidHoltom-Garrett Program in Neuroimmunology, Department of Neurology.
Benjamin M SegalHoltom-Garrett Program in Neuroimmunology, Department of Neurology.
Institute of Neuroimmunology of the Slovak Academy of Sciences · SKUniversity of Michigan · USVA Ann Arbor Healthcare System · US

Funding

MICHIGAN MEDICAL SCIENTIST TRAINING PROGRAMT32GM007863 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI COLLINS, KATHLEEN L. · 1985 to 2024
$38.3M
RESEARCH TRAINING IN EXPERIMENTAL IMMUNOPATHOLOGYT32AI007413 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Bethany B. Moore · 1993 to 2026
$9.8M
Arginase-1 and iNOS expressing CNS myeloid cell subsets in EAE and MSR01NS105385 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SEGAL, BENJAMIN M · 2017 to 2021
$1.9M
The mechanism of action of Granulocyte Macrophage-Colony Stimulating Factor in an animal model of Multiple SclerosisR21NS103215 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SEGAL, BENJAMIN M · 2017 to 2018
$427k
NIAID NIH HHS T32 AI007413NIGMS NIH HHS T32 GM007863NINDS NIH HHS R01 NS105385NINDS NIH HHS R21 NS103215
6 · The paper itself

Abstract

Experimental autoimmune encephalomyelitis (EAE) is an inflammatory demyelinating disease of the central nervous system (CNS), induced by the adoptive transfer of myelin-reactive CD4+ T cells into naive syngeneic mice. It is widely used as a rodent model of multiple sclerosis (MS). The development of EAE lesions is initiated when transferred CD4+ T cells access the CNS and are reactivated by local antigen-presenting cells (APCs) bearing endogenous myelin peptide/MHC class II complexes. The identity of the CNS-resident, lesion-initiating APCs is widely debated. Here we demonstrate that classical dendritic cells (cDCs) normally reside in the meninges, brain, and spinal cord in the steady state. These cells are unique among candidate CNS APCs in their ability to stimulate naive, as well as effector, myelin-specific T cells to proliferate and produce proinflammatory cytokines directly ex vivo. cDCs expanded in the meninges and CNS parenchyma in association with disease progression. Selective depletion of cDCs led to a decrease in the number of myelin-primed donor T cells in the CNS and reduced the incidence of clinical EAE by half. Based on our findings, we propose that cDCs, and the factors that regulate them, be further investigated as potential therapeutic targets in MS.

Indexed as

Adoptive TransferAnimalsAntigen PresentationBrainCD4-Positive T-LymphocytesCytokinesDendritic CellsEncephalomyelitis, Autoimmune, ExperimentalLymphocyte ActivationMiceMice, TransgenicMyelin-Oligodendrocyte GlycoproteinSpinal CordCytokinesMyelin-Oligodendrocyte GlycoproteinAntigen presenting cellsAutoimmune diseasesAutoimmunityMultiple sclerosisNeuroscience

Identifiers

PMID30226829
PMCPMC6264723
OpenAlexW2889831587

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.