Evidence map›Paper›PMID 27704036›Full record

ArticleNeurology(R) neuroimmunology & neuroinflammation2016

Treatment of spontaneous EAE by laquinimod reduces Tfh, B cell aggregates, and disease progression.

Michel Varrin-Doyer, Kara L Pekarek, Collin M Spencer, Claude C A Bernard, Raymond A Sobel, Bruce A C Cree, Ulf Schulze-Topphoff, Scott S Zamvil

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neurology(R) neuroimmunology & neuroinflammation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

28 citing papers in PubMed, 43 citations in OpenAlex.

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  10. Treatment with an antigen-specific dual microparticle system reverses advanced multiple sclerosis in mice.Proceedings of the National Academy of Sciences of the United States of America · 2022
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  16. Follicular Helper CD4Mediators of inflammation · 2021
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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 2 institutions in 1 country.

Michel Varrin-DoyerDepartment of Neurology (M.V.-D., K.L.P., C.M.S., B.A.C.C., U.S.-T., S.S.Z.) and Program in Immunology (M.V.-D., K.L.P., C.M.S., U.S.-T., S.S.Z.), University of California, San Francisco; Multiple Sclerosis Research Group (C.C.A.B.), Australian Regenerative Medicine Institute, Monash University, Clayton, Australia; and Department of Pathology (R.A.S.), Stanford University, CA.
Kara L PekarekDepartment of Neurology (M.V.-D., K.L.P., C.M.S., B.A.C.C., U.S.-T., S.S.Z.) and Program in Immunology (M.V.-D., K.L.P., C.M.S., U.S.-T., S.S.Z.), University of California, San Francisco; Multiple Sclerosis Research Group (C.C.A.B.), Australian Regenerative Medicine Institute, Monash University, Clayton, Australia; and Department of Pathology (R.A.S.), Stanford University, CA.
Collin M SpencerDepartment of Neurology (M.V.-D., K.L.P., C.M.S., B.A.C.C., U.S.-T., S.S.Z.) and Program in Immunology (M.V.-D., K.L.P., C.M.S., U.S.-T., S.S.Z.), University of California, San Francisco; Multiple Sclerosis Research Group (C.C.A.B.), Australian Regenerative Medicine Institute, Monash University, Clayton, Australia; and Department of Pathology (R.A.S.), Stanford University, CA.
Claude C A BernardDepartment of Neurology (M.V.-D., K.L.P., C.M.S., B.A.C.C., U.S.-T., S.S.Z.) and Program in Immunology (M.V.-D., K.L.P., C.M.S., U.S.-T., S.S.Z.), University of California, San Francisco; Multiple Sclerosis Research Group (C.C.A.B.), Australian Regenerative Medicine Institute, Monash University, Clayton, Australia; and Department of Pathology (R.A.S.), Stanford University, CA.
Raymond A SobelDepartment of Neurology (M.V.-D., K.L.P., C.M.S., B.A.C.C., U.S.-T., S.S.Z.) and Program in Immunology (M.V.-D., K.L.P., C.M.S., U.S.-T., S.S.Z.), University of California, San Francisco; Multiple Sclerosis Research Group (C.C.A.B.), Australian Regenerative Medicine Institute, Monash University, Clayton, Australia; and Department of Pathology (R.A.S.), Stanford University, CA.
Bruce A C CreeDepartment of Neurology (M.V.-D., K.L.P., C.M.S., B.A.C.C., U.S.-T., S.S.Z.) and Program in Immunology (M.V.-D., K.L.P., C.M.S., U.S.-T., S.S.Z.), University of California, San Francisco; Multiple Sclerosis Research Group (C.C.A.B.), Australian Regenerative Medicine Institute, Monash University, Clayton, Australia; and Department of Pathology (R.A.S.), Stanford University, CA.
Ulf Schulze-TopphoffDepartment of Neurology (M.V.-D., K.L.P., C.M.S., B.A.C.C., U.S.-T., S.S.Z.) and Program in Immunology (M.V.-D., K.L.P., C.M.S., U.S.-T., S.S.Z.), University of California, San Francisco; Multiple Sclerosis Research Group (C.C.A.B.), Australian Regenerative Medicine Institute, Monash University, Clayton, Australia; and Department of Pathology (R.A.S.), Stanford University, CA.
Scott S ZamvilDepartment of Neurology (M.V.-D., K.L.P., C.M.S., B.A.C.C., U.S.-T., S.S.Z.) and Program in Immunology (M.V.-D., K.L.P., C.M.S., U.S.-T., S.S.Z.), University of California, San Francisco; Multiple Sclerosis Research Group (C.C.A.B.), Australian Regenerative Medicine Institute, Monash University, Clayton, Australia; and Department of Pathology (R.A.S.), Stanford University, CA.
Australian Regenerative Medicine Institute · AUMonash University · AU

Funding

B cells in CNS autoimmunityR01AI073737 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI ZAMVIL, SCOTT S · 2009 to 2013
$1.9M
NIAID NIH HHS R01 AI073737
6 · The paper itself

Abstract

objectiveTo evaluate the influence of oral laquinimod, a candidate multiple sclerosis (MS) treatment, on induction of T follicular helper cells, development of meningeal B cell aggregates, and clinical disease in a spontaneous B cell-dependent MS model.

methodsExperimental autoimmune encephalomyelitis (EAE) was induced in C57BL/6 mice by immunization with recombinant myelin oligodendrocyte glycoprotein (rMOG) protein. Spontaneous EAE was evaluated in C57BL/6 MOG p35-55-specific T cell receptor transgenic (2D2) × MOG-specific immunoglobulin (Ig)H-chain knock-in (IgH

resultsOral laquinimod treatment (1) reduced CD11c

conclusionsOur observations that laquinimod modulates myelin antigen-specific B cell immune responses and suppresses both development of meningeal B cell aggregates and disability progression in spontaneous EAE should provide insight regarding the potential application of laquinimod to MS treatment. Results of this investigation demonstrate how the 2D2 × Th spontaneous EAE model can be used successfully for preclinical evaluation of a candidate MS treatment.

Identifiers

PMID27704036
PMCPMC5032667
OpenAlexW2522200429

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.