Evidence map›Paper›PMID 20217033›Full record

ReviewJournal of molecular medicine (Berlin, Germany)2010

The role of dendritic cells in CNS autoimmunity.

Alla L Zozulya, Benjamin D Clarkson, Sonja Ortler, Zsuzsanna Fabry, Heinz Wiendl

Open access · greenAbstract readReview
In one paragraph

Review in Journal of molecular medicine (Berlin, Germany), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
4.2field-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

43 citing papers in PubMed, 78 citations in OpenAlex.

  1. Paradoxical Expression of Ionotropic Glutamate Receptors in Leucocytes.Clinical reviews in allergy & immunology · 2026
    Article
  2. Frontiers in cellular neuroscience · 2026
    Review
  3. Review
  4. Review
  5. Botanically-Derived ΔMolecules (Basel, Switzerland) · 2022
    Article
  6. Article
  7. Review
  8. Article
  9. Dopaminergic Therapeutics in Multiple Sclerosis: Focus on Th17-Cell Functions.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2020
    Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Increase of Alternatively Activated Antigen Presenting Cells in Active Experimental Autoimmune Encephalomyelitis.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2016
    Article
  17. Alemtuzumab treatment alters circulating innate immune cells in multiple sclerosis.Neurology(R) neuroimmunology & neuroinflammation · 2016
    Article
  18. Review
  19. Article
  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

5 authors at 3 institutions in 3 countries.

Alla L ZozulyaDepartment of Immunology, University of Geneva, Rue Gabrielle-Perret-Gentil 4, 1211, Genève, 14, Switzerland.
Benjamin D Clarkson
Sonja Ortler
Zsuzsanna Fabry
Heinz Wiendl
University of Wisconsin–Madison · USUniversity of Würzburg · DEUniversity of Geneva · CH

Funding

ANTIGEN SPECIFIC T CELL ACCUMULATION IN THE CNSR01NS037570 · NINDS · UNIVERSITY OF WISCONSIN-MADISON · PI FABRY, ZSUZSANNA · 2000 to 2012
$3.1M
Antigen specific T cell accumulation in the CNSR56NS037570 · NINDS · UNIVERSITY OF WISCONSIN-MADISON · PI FABRY, ZSUZSANNA · 2008 to 2008
$367k
NINDS NIH HHS R01 NS037570NINDS NIH HHS R56 NS037570
6 · The paper itself

Abstract

Multiple sclerosis (MS) is a chronic immune-mediated, central nervous system (CNS) demyelinating disease. Clinical and histopathological features suggest an inflammatory etiology involving resident CNS innate cells as well as invading adaptive immune cells. Encephalitogenic myelin-reactive T cells have been implicated in the initiation of an inflammatory cascade, eventually resulting in demyelination and axonal damage (the histological hallmarks of MS). Dendritic cells (DC) have recently emerged as key modulators of this immunopathological cascade, as supported by studies in humans and experimental disease models. In one such model, experimental autoimmune encephalomyelitis (EAE), CNS microvessel-associated DC have been shown to be essential for local antigen recognition by myelin-reactive T cells. Moreover, the functional state and compartmental distribution of DC derived from CNS and associated lymphatics seem to be limiting factors in both the induction and effector phases of EAE. Moreover, DC modulate and balance the recruitment of encephalitogenic and regulatory T cells into CNS tissue. This capacity is critically influenced by DC surface expression of co-stimulatory or co-inhibitory molecules. The fact that DC accumulate in the CNS before T cells and can direct T-cell responses suggests that they are key determinants of CNS autoimmune outcomes. Here we provide a comprehensive review of recent advances in our understanding of CNS-derived DC and their relevance to neuroinflammation.

Indexed as

Adaptive ImmunityAnimalsAntigens, CDAutoimmunityB7-H1 AntigenCentral Nervous SystemDendritic CellsEncephalomyelitis, Autoimmune, ExperimentalHumansImmunity, InnateMultiple SclerosisT-LymphocytesAntigens, CDB7-H1 AntigenCD274 protein, human

Identifiers

PMID20217033
PMCPMC2869392
OpenAlexW2099166441

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.