Evidence map›Paper›PMID 23079547›Full record

ArticleNeuroscience letters2012

Targeted inhibition of complement using complement receptor 2-conjugated inhibitors attenuates EAE.

Xianzhen Hu, Stephen Tomlinson, Scott R Barnum

Abstract read
In one paragraph

Article in Neuroscience letters, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.1field-weighted citation impact, top 49% 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

17 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
  2. Towards Treating Multiple Sclerosis Progression.Pharmaceuticals (Basel, Switzerland) · 2024
    Review
  3. Review
  4. The complement system in neurodegenerative diseases.Clinical science (London, England : 1979) · 2024
    Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Complement C3-Targeted Gene Therapy Restricts Onset and Progression of Neurodegeneration in Chronic Mouse Glaucoma.Molecular therapy : the journal of the American Society of Gene Therapy · 2018
    Article
  14. Tissue-targeted complement therapeutics.Molecular immunology · 2018
    Review
  15. Article
  16. Article
  17. 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

3 authors at 2 institutions in 1 country.

Xianzhen HuDepartment of Microbiology, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Stephen Tomlinson
Scott R Barnum
University of Alabama at Birmingham · USMedical University of South Carolina · US

Funding

Controlling complement in cerebral ischemic injuryR01HL082485 · NHLBI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI TOMLINSON, STEPHEN · 2006 to 2010
$1.6M
Complement-based Therapeutics in Demyelinating DiseaseR21NS069365 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BARNUM, SCOTT R · 2010 to 2011
$403k
NHLBI NIH HHS HL082485NHLBI NIH HHS R01 HL082485NINDS NIH HHS NS069365NINDS NIH HHS R21 NS069365
6 · The paper itself

Abstract

Multiple sclerosis (MS) is the most common autoimmune demyelinating disease, affecting millions of individuals worldwide. In the last two decades, many therapeutic options for the treatment of MS have become available, however they are limited in terms of effectiveness and some remain plagued by safety issues. The currently available treatment options target relapsing remitting forms of MS and are not effective against the more progressive forms of the disease. These limitations highlight a significant unmet treatment need for MS. In experimental autoimmune encephalomyelitis (EAE) studies from our laboratory, we have previously shown, using a number of complement mutant and transgenic mice, that inhibition of the alternative complement pathway and the C3 convertase confers significant protection from disease. We report here that targeted inhibition of complement activation using complement receptor 2 (CR2)-conjugated inhibitors significantly attenuates EAE. Administration of CR2-Crry (blocks all complement pathways at C3 activation) and CR2-fH (specifically blocks the alternative pathway) just prior to and during the onset of EAE blocks progression of both acute and chronic disease. These data indicate that inhibition of complement may offer an effective therapeutic approach to treating both acute and chronic forms of demyelinating disease through blocking the alternative pathway or complement convertases.

Indexed as

AnimalsComplement Inactivating AgentsComplement Pathway, AlternativeDisease Models, AnimalEncephalomyelitis, Autoimmune, ExperimentalMiceMice, Inbred C57BLMolecular Targeted TherapyReceptors, Complement 3dRecombinant Fusion ProteinsComplement Inactivating AgentsCR2-Crry fusion protein, mouseReceptors, Complement 3dRecombinant Fusion Proteins

Identifiers

PMID23079547
PMCPMC3498843
OpenAlexW1996932281

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.