Evidence map›Paper›PMID 24196276›Full record

ArticleJournal of neuroimmunology2014

In trans T cell tolerance exacerbates experimental allergic encephalomyelitis by interfering with protective antibody responses.

Jason A Cascio, Marie-Therese Khairallah, Xiaoxiao Wan, Weirong Chen, Linda M Rowland, Mermagya Dhakal, Mindy M Miller, Habib Zaghouani

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

Article in Journal of neuroimmunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact, top 91% 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

0 citing papers in PubMed, 1 citations in OpenAlex.

No citing paper in PubMed yet.

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 1 institution in 1 country.

Jason A CascioDepartment of Molecular Microbiology and Immunology, University of Missouri School of Medicine, M616 Medical Sciences Building, Columbia, MO 65212, USA.
Marie-Therese KhairallahDepartment of Molecular Microbiology and Immunology, University of Missouri School of Medicine, M616 Medical Sciences Building, Columbia, MO 65212, USA.
Xiaoxiao WanDepartment of Molecular Microbiology and Immunology, University of Missouri School of Medicine, M616 Medical Sciences Building, Columbia, MO 65212, USA.
Weirong ChenDepartment of Molecular Microbiology and Immunology, University of Missouri School of Medicine, M616 Medical Sciences Building, Columbia, MO 65212, USA.
Linda M RowlandDepartment of Molecular Microbiology and Immunology, University of Missouri School of Medicine, M616 Medical Sciences Building, Columbia, MO 65212, USA.
Mermagya DhakalDepartment of Molecular Microbiology and Immunology, University of Missouri School of Medicine, M616 Medical Sciences Building, Columbia, MO 65212, USA.
Mindy M MillerDepartment of Molecular Microbiology and Immunology, University of Missouri School of Medicine, M616 Medical Sciences Building, Columbia, MO 65212, USA.
Habib ZaghouaniDepartment of Molecular Microbiology and Immunology, University of Missouri School of Medicine, M616 Medical Sciences Building, Columbia, MO 65212, USA; Department of Child Health, University of Missouri School of Medicine, M616 Medical Sciences Building, Columbia, MO 65212, USA; Department of Neurology, University of Missouri School of Medicine, M616 Medical Sciences Building, Columbia, MO 65212, USA. Electronic address: zaghouanih@health.missouri.edu.
University of Missouri · US

Funding

Regulation of Autoimmune EncephalomyelitisR01NS057194 · NINDS · UNIVERSITY OF MISSOURI-COLUMBIA · PI ZAGHOUANI, HABIB · 2008 to 2017
$2.9M
NINDS NIH HHS R01 NS057194
6 · The paper itself

Abstract

F1 (SJL/J×C57BL/6) mice with MOG35-55-induced EAE recover from disease when treated with Ig-MOG carrying MOG35-55 peptide. However, Ig-PLP1, carrying PLP139-151, induced reduction of anti-MOG antibodies and exacerbated EAE. Herein, we show that Ig-PLP1 specifically reduces the frequency of B cells producing protective IgG2a/b anti-MOG antibodies. Surprisingly, these cells were marginal zone (MZ), rather than follicular (FO) or newly formed (NF), B cells and transfer of MZ B cells into sick mice nullified disease exacerbation by Ig-PLP1 in a complement dependent manner. These findings reveal a potential self-limiting regulatory mechanism involving auto-antibodies in MOG EAE.

Indexed as

AnimalsAntibodiesB-LymphocytesCytokinesDisease Models, AnimalEncephalomyelitis, Autoimmune, ExperimentalEnzyme-Linked Immunosorbent AssayFemaleFlow CytometryImmune ToleranceLymphocyte ActivationMiceMice, Inbred C57BLMyelin-Oligodendrocyte GlycoproteinPeptide FragmentsStatistics, NonparametricAntibodiesCytokinesMyelin-Oligodendrocyte Glycoproteinmyelin oligodendrocyte glycoprotein (35-55)Peptide FragmentsAnti-MOG antibodiesAutoimmunityB cellsEAET cell tolerance

Identifiers

PMID24196276
PMCPMC4762480
OpenAlexW2042038229

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.