Evidence map›Paper›PMID 17493037›Full record

ArticleBrain pathology (Zurich, Switzerland)2007

Modulation of experimental autoimmune encephalomyelitis by VLA-2 blockade.

Ikuo Tsunoda, Emily Jane Terry, Benjamin J Marble, Elias Lazarides, Catherine Woods, Robert S Fujinami

Open access · greenAbstract read
In one paragraph

Article in Brain pathology (Zurich, Switzerland), 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.5field-weighted citation impact, top 21% 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

20 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
  2. Article
  3. What Have Failed, Interrupted, and Withdrawn Antibody Therapies in Multiple Sclerosis Taught Us?Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022
    Review
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  5. Metallothionein I as a direct link between therapeutic hematopoietic stem/progenitor cells and cerebral protection in stroke.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018
    Article
  6. Article
  7. Article
  8. Neuroimmunotherapies Targeting T Cells: From Pathophysiology to Therapeutic Applications.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2016
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Integrin signaling in cancer cell survival and chemoresistance.Chemotherapy research and practice · 2012
    Article
  14. Article
  15. Neuropathogenesis of Theiler's murine encephalomyelitis virus infection, an animal model for multiple sclerosis.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2010
    Review
  16. The importance of NAD in multiple sclerosis.Current pharmaceutical design · 2009
    Review
  17. Article
  18. Innovative monoclonal antibody therapies in multiple sclerosis.Therapeutic advances in neurological disorders · 2008
    Article
  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

6 authors at 1 institution in 1 country.

Ikuo TsunodaDepartment of Neurology, University of Utah School of Medicine, Salt Lake City, Utah 84132-2305, USA.
Emily Jane Terry
Benjamin J Marble
Elias Lazarides
Catherine Woods
Robert S Fujinami
University of Utah · US

Funding

Immunologic Factors In Progressive Autoimmune DiseaseR01NS040350 · NINDS · UNIVERSITY OF UTAH · PI FUJINAMI, ROBERT S · 2002 to 2005
$998k
NINDS NIH HHS 5 R01 NS40350NINDS NIH HHS R01 NS040350
6 · The paper itself

Abstract

Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system (CNS). Adhesion molecules play important roles in cell-cell and cell-extracellular matrix (ECM) interactions in inflammation. Blocking the interaction between inflammatory cells and vascular endothelia can prevent cell entry into tissues and harmful inflammatory responses, that is, autoimmunity, but could also limit immunosurveillance by anti-viral T cells in sites of infection or latency. Development of progressive multifocal leukoencephalopathy in patients treated with antibody against very late antigen (VLA)-4 prompted us to explore an alternative therapeutic approach. We used an antibody against the integrin alpha2, VLA-2, that interacts with ECM, not vascular endothelium. SJL/J mice were sensitized with myelin proteolipid protein (PLP)(139-151) peptide to induce experimental autoimmune encephalomyelitis (EAE), an animal model for MS. Treatment of mice with VLA-2 antibody suppressed clinical signs and CNS inflammation of EAE, when antibody was given immediately after disease onset. In contrast, VLA-4 or VLA-2 antibody treatment of mice during the priming or remission phase of EAE had minor effects on the disease's clinical course. No differences were found in lymphoproliferative responses to PLP(139-151) among treatment groups. Data suggest that blocking cell-ECM interactions can be an alternative therapy for MS.

Indexed as

AnimalsAntibodies, MonoclonalCentral Nervous SystemDisease Models, AnimalDrug Administration ScheduleEncephalomyelitis, Autoimmune, ExperimentalFemaleIntegrin alpha2beta1Integrin alpha4beta1MiceMultiple SclerosisAntibodies, MonoclonalIntegrin alpha2beta1Integrin alpha4beta1

Identifiers

PMID17493037
PMCPMC8095550
OpenAlexW2019927335

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.