Evidence map›Paper›PMID 26489686›Full record

ArticleASN neuro

A Distinct Class of Antibodies May Be an Indicator of Gray Matter Autoimmunity in Early and Established Relapsing Remitting Multiple Sclerosis Patients.

Ann J Ligocki, Jacqueline R Rivas, William H Rounds, Alyssa A Guzman, Min Li, Melania Spadaro, Lauren Lahey, Ding Chen, Paul M Henson, Donna Graves and 8 more

Open access · goldAbstract read
In one paragraph

Article in ASN neuro. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

13 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
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  8. Black African and Latino/a identity correlates with increased plasmablasts in MS.Neurology(R) neuroimmunology & neuroinflammation · 2020
    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

18 authors at 3 institutions in 2 countries.

Ann J LigockiDepartment of Neurology and Neurotherapeutics, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Jacqueline R RivasDepartment of Neurology and Neurotherapeutics, University of Texas Southwestern Medical Center, Dallas, TX, USA.
William H RoundsDepartment of Neurology and Neurotherapeutics, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Alyssa A GuzmanDepartment of Neurology and Neurotherapeutics, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Min LiDepartment of Neurology and Neurotherapeutics, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Melania SpadaroInstitute of Clinical Neuroimmunology, Ludwig-Maximilian-University, Munich, Germany.
Lauren LaheyDepartment of Immunology and Rheumatology, Stanford University, CA, USA.
Ding ChenDepartment of Neurology and Neurotherapeutics, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Paul M HensonDepartment of Neurology and Neurotherapeutics, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Donna GravesDepartment of Neurology and Neurotherapeutics, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Benjamin M GreenbergDepartment of Neurology and Neurotherapeutics, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Elliot M FrohmanDepartment of Neurology and Neurotherapeutics, University of Texas Southwestern Medical Center, Dallas, TX, USA.
E Sally WardDepartment of Immunology, University of Texas Southwestern Medical Center, Dallas, TX, USA.
William RobinsonDepartment of Immunology and Rheumatology, Stanford University, CA, USA.
Edgar MeinlInstitute of Clinical Neuroimmunology, Ludwig-Maximilian-University, Munich, Germany.
Charles L WhiteDepartment of Pathology, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Ann M StoweDepartment of Neurology and Neurotherapeutics, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Nancy L MonsonDepartment of Neurology and Neurotherapeutics, University of Texas Southwestern Medical Center, Dallas, TX, USA Department of Immunology, University of Texas Southwestern Medical Center, Dallas, TX, USA nancy.monson@utsouthwestern.edu.
The University of Texas Southwestern Medical Center · USLudwig-Maximilians-Universität München · DEStanford University · US

Funding

INTEGRATIVE IMMUNOLOGY TRAINING PROGRAMT32AI005284 · NIAID · UT SOUTHWESTERN MEDICAL CENTER · PI Nan Yan · 2003 to 2026
$7.4M
NIAID NIH HHS T32 AI005284NINDS NIH HHS L30 NS084459PHS HHS 5 T32 A1 005284-28
6 · The paper itself

Abstract

*These authors contributed equally to the work in this manuscript.We have previously identified a distinct class of antibodies expressed by B cells in the cerebrospinal fluid (CSF) of early and established relapsing remitting multiple sclerosis (RRMS) patients that is not observed in healthy donors. These antibodies contain a unique pattern of mutations in six codons along VH4 antibody genes that we termed the antibody gene signature (AGS). In fact, patients who have such B cells in their CSF are identified as either having RRMS or developing RRMS in the future. As mutations in antibody genes increase antibody affinity for particular antigens, the goal for this study was to investigate whether AGS(+) antibodies bind to brain tissue antigens. Single B cells were isolated from the CSF of 10 patients with early or established RRMS. We chose 32 of these B cells that expressed antibodies enriched for the AGS for further study. We generated monoclonal full-length recombinant human antibodies (rhAbs) and used both immunological assays and immunohistochemistry to investigate the capacity of these AGS(+) rhAbs to bind brain tissue antigens. AGS(+) rhAbs did not recognize myelin tracts in the corpus callosum. Instead, AGS(+) rhAbs recognized neuronal nuclei and/or astrocytes, which are prevalent in the cortical gray matter. This pattern was unique to the AGS(+) antibodies from early and established RRMS patients, as AGS(+) antibodies from an early neuromyelitis optica patient did not display the same reactivity. Prevalence of CSF-derived B cells expressing AGS(+) antibodies that bind to these cell types may be an indicator of gray matter-directed autoimmunity in early and established RRMS patients.

Indexed as

AdultAnimalsAutoantibodiesAutoimmunityB-LymphocytesBrainEncephalomyelitis, Autoimmune, ExperimentalFemaleGlycoproteinsGray MatterHeLa CellsHumansMaleMiceMice, TransgenicMiddle AgedAutoantibodiesGlycoproteinsRecombinant ProteinsautoantibodyB cellclinically isolated syndromegray mattermultiple sclerosismyelin tracts

Identifiers

PMID26489686
PMCPMC4710131
OpenAlexW2173821929

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.