Evidence map›Paper›PMID 21095100›Full record

ArticleJournal of autoimmunity2011

Limited sufficiency of antigen presentation by dendritic cells in models of central nervous system autoimmunity.

Gregory F Wu, Kenneth S Shindler, Eric J Allenspach, Tom L Stephen, Hannah L Thomas, Robert J Mikesell, Anne H Cross, Terri M Laufer

Open access · greenAbstract read
In one paragraph

Article in Journal of autoimmunity, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

33 citing papers in PubMed, 51 citations in OpenAlex.

  1. Turncoat antibodies unmasked in a model of autoimmune demyelination: From biology to therapy.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  2. Role of dendritic cells in spinal cord injury.CNS neuroscience & therapeutics · 2024
    Review
  3. Article
  4. Review
  5. Antigen-specific depletion of CD4Science immunology · 2022
    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

8 authors at 3 institutions in 1 country.

Gregory F WuDepartment of Neurology, University of Pennsylvania School of Medicine, Philadelphia, PA 19004, USA. wug@neuro.wustl.edu
Kenneth S Shindler
Eric J Allenspach
Tom L Stephen
Hannah L Thomas
Robert J Mikesell
Anne H Cross
Terri M Laufer
University of Pennsylvania · USWashington University in St. Louis · USVeterans Health Administration · US

Funding

Mechanism of SIRT1 Activator Mediated Neuroprotection of Retinal Ganglion CellsR01EY019014 · NEI · UNIVERSITY OF PENNSYLVANIA · PI SHINDLER, KENNETH S · 2010 to 2020
$3.7M
Thymocyte tuning after selection: mechanisms to avoid autoreactivityR01AI068819 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI LAUFER, TERRI M. · 2007 to 2010
$1.5M
T cell regulation by dendritic cells in EAEK08NS062138 · NINDS · WASHINGTON UNIVERSITY · PI WU, GREGORY · 2008 to 2012
$831k
NEI NIH HHS R01 EY019014NIAID NIH HHS R01 AI068819NINDS NIH HHS K08 NS062138
6 · The paper itself

Abstract

Experimental autoimmune encephalomyelitis (EAE), a model for the human disease multiple sclerosis (MS), is dependent upon the activation and effector functions of autoreactive CD4 T cells. Multiple interactions between CD4 T cells and major histocompatibility class II (MHCII)+ antigen presenting cells (APCs) must occur in both the periphery and central nervous system (CNS) to elicit autoimmunity. The identity of the MHCII+ APCs involved throughout this process remains in question. We investigated which APC in the periphery and CNS mediates disease using transgenic mice with MHCII expression restricted to dendritic cells (DCs). MHCII expression restricted to DCs results in normal susceptibility to peptide-mediated EAE. Indeed, radiation-sensitive bone marrow-derived DCs were sufficient for all APC functions during peptide-induced disease. However, DCs alone were inefficient at promoting disease after immunization with the myelin protein myelin oligodendrocyte glycoprotein (MOG), even in the presence of MHCII-deficient B cells. Consistent with a defect in disease induction following protein immunization, antigen presentation by DCs alone was incapable of mediating spontaneous optic neuritis. These results indicate that DCs are capable of perpetuating CNS-targeted autoimmunity when antigens are readily available, but other APCs are required to efficiently initiate pathogenic cognate CD4 T cell responses.

Indexed as

AnimalsAntigen PresentationCD4-Positive T-LymphocytesCell SeparationDendritic CellsEncephalomyelitis, Autoimmune, ExperimentalEnzyme-Linked Immunosorbent AssayFlow CytometryHistocompatibility Antigens Class IILymphocyte ActivationMiceMice, Inbred C57BLMice, TransgenicOptic NerveSpinal CordHistocompatibility Antigens Class II

Identifiers

PMID21095100
PMCPMC3053076
OpenAlexW2166059415

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.