Evidence map›Paper›PMID 20637861›Full record

ReviewBiochimica et biophysica acta2011

The role of antigen presenting cells in multiple sclerosis.

Emily M L Chastain, D'Anne S Duncan, Jane M Rodgers, Stephen D Miller

Open access · greenAbstract readReview
In one paragraph

Review in Biochimica et biophysica acta, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 143 papers.

0numbers the graph read from it
0cells of the map it votes in
143citing papers in PubMed
6.2field-weighted citation impact, top 3% 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

143 citing papers in PubMed, 263 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Role of isoflavones in multiple sclerosis.IBRO neuroscience reports · 2025
    Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Immune-responsive gene 1: The mitochondrial key to Th17 cell pathogenicity in CNS autoimmunity.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Review
  19. Astrocyte Activation and Drug Target in Pathophysiology of Multiple Sclerosis.Methods in molecular biology (Clifton, N.J.) · 2024
    Review
  20. Article

83 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 1 country.

Emily M L ChastainDepartment of Microbiology-Immunology, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA.
D'Anne S Duncan
Jane M Rodgers
Stephen D Miller
Northwestern University · US

Funding

IMMUNOREGULATION AND PATHOLOGY OF CHRONIC-RELAPSING EAER01NS026543 · NINDS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI MILLER, STEPHEN D · 1988 to 2016
$5.0M
PATHOGENESIS AND IMMUNOREGULATION OF PLP-INDUCED R-EAER01NS030871 · NINDS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI MILLER, STEPHEN D · 1993 to 2010
$3.4M
Innate Regulation and CD4+Th1/17 Immunity in TMEV-Induced DemyelinationR01NS062365 · NINDS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI MILLER, STEPHEN D · 2010 to 2014
$1.6M
Training Program in Viral ReplicationT32AI060523 · NIAID · NORTHWESTERN UNIVERSITY AT CHICAGO · PI LAIMINS, LAIMONIS A. · 2004 to 2013
$1.4M
Training for a New Interdisciplinary Research Workforce in Regenerative MedicineT90DA022881 · NIDA · NORTHWESTERN UNIVERSITY AT CHICAGO · PI KESSLER, JOHN A · 2006 to 2009
$1.1M
The Role of Microglia during TMEV-IDD in the Adult MouseF31NS061621 · NINDS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI DUNCAN, D'ANNE S. · 2008 to 2010
$65k
NIAID NIH HHS T32 AI060523NIAID NIH HHS T32 AI060523-06NIDA NIH HHS T90 DA022881NINDS NIH HHS F31 NS061621NINDS NIH HHS R01 NS026543NINDS NIH HHS R01 NS030871NINDS NIH HHS R01 NS062365
6 · The paper itself

Abstract

Multiple sclerosis (MS) is a debilitating T cell mediated autoimmune disease of the central nervous system (CNS). Animal models of MS, such as experimental autoimmune encephalomyelitis (EAE) and Theiler's murine encephalomyelitis virus-induced demyelinating disease (TMEV-IDD) have given light to cellular mechanisms involved in the initiation and progression of this organ-specific autoimmune disease. Within the CNS, antigen presenting cells (APC) such as microglia and astrocytes participate as first line defenders against infections or inflammation. However, during chronic inflammation they can participate in perpetuating the self-destructive environment by secretion of inflammatory factors and/or presentation of myelin epitopes to autoreactive T cells. Dendritic cells (DC) are also participants in the presentation of antigen to T cells, even within the CNS. While the APCs alone are not solely responsible for mediating the destruction to the myelin sheath, they are critical players in perpetuating the inflammatory milieu. This review will highlight relevant studies which have provided insight to the roles played by microglia, DCs and astrocytes in the context of CNS autoimmunity.

Indexed as

AnimalsAntigen PresentationAntigen-Presenting CellsAstrocytesCardiovirus InfectionsCytokinesDemyelinating DiseasesDendritic CellsEncephalomyelitis, Autoimmune, ExperimentalHumansMacrophagesMajor Histocompatibility ComplexMiceMicrogliaMultiple SclerosisTheilovirusCytokinesToll-Like Receptors

Identifiers

PMID20637861
PMCPMC2970677
OpenAlexW2116041320

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.