Evidence map›Paper›PMID 10841576›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2000

Human monoclonal antibodies reactive to oligodendrocytes promote remyelination in a model of multiple sclerosis.

A E Warrington, K Asakura, A J Bieber, B Ciric, V Van Keulen, S V Kaveri, R A Kyle, L R Pease, M Rodriguez

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.

0numbers the graph read from it
0cells of the map it votes in
92citing papers in PubMed
6.3field-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

92 citing papers in PubMed, 256 citations in OpenAlex.

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32 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

9 authors at 2 institutions in 2 countries.

A E WarringtonDepartments of Neurology, Immunology, and Hematology, Mayo Medical and Graduate Schools, Rochester, MN 55905, USA.
K Asakura
A J Bieber
B Ciric
V Van Keulen
S V Kaveri
R A Kyle
L R Pease
M Rodriguez
Inserm · FRNagoya University · JP

Funding

IMMUNE PROMOTION OF REMYELINATIONR01NS024180 · NINDS · MAYO CLINIC ROCHESTER · PI RODRIGUEZ, MOSES · 1987 to 2008
$2.7M
NINDS NIH HHS NS24180NINDS NIH HHS R01 NS024180
6 · The paper itself

Abstract

Promoting remyelination, a major goal of an effective treatment for demyelinating diseases, has the potential to protect vulnerable axons, increase conduction velocity, and improve neurologic deficits. Strategies to promote remyelination have focused on transplanting oligodendrocytes (OLs) or recruiting endogenous myelinating cells with trophic factors. Ig-based therapies, routinely used to treat a variety of neurological and autoimmune diseases, underlie our approach to enhance remyelination. We isolated two human mAbs directed against OL surface antigens that promoted significant remyelination in a virus-mediated model of multiple sclerosis. Four additional OL-binding human mAbs did not promote remyelination. Both human mAbs were as effective as human i.v. Ig, a treatment shown to have efficacy in multiple sclerosis, and bound to the surface of human OLs suggesting a direct effect of the mAbs on the cells responsible for myelination. Alternatively, targeting human mAbs to areas of central nervous system (CNS) pathology may facilitate the opsonization of myelin debris, allowing repair to proceed. Human mAbs were isolated from the sera of individuals with a form of monoclonal gammopathy. These individuals carry a high level of monoclonal protein in their blood without detriment, lending support to the belief that administration of these mAbs as a therapy would be safe. Our results are (i) consistent with the hypothesis that CNS-reactive mAbs, part of the normal Ig repertoire in humans, may help repair and protect the CNS from pathogenic immune injury, and (ii) further challenge the premise that Abs that bind OLs are necessarily pathogenic.

Indexed as

Antibodies, MonoclonalBase SequenceHumansImmunoglobulin MImmunoglobulins, IntravenousMolecular Sequence DataMultiple SclerosisMyelin SheathOligodendrogliaPoliomyelitisTheilovirusAntibodies, MonoclonalImmunoglobulin MImmunoglobulins, Intravenous

Identifiers

PMID10841576
PMCPMC18751
OpenAlexW1998253454

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.