Evidence map›Paper›PMID 9653093›Full record

ArticleThe Journal of experimental medicine1998

B lymphocytes producing demyelinating autoantibodies: development and function in gene-targeted transgenic mice.

T Litzenburger, R Fässler, J Bauer, H Lassmann, C Linington, H Wekerle, A Iglesias

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers.

0numbers the graph read from it
0cells of the map it votes in
99citing papers in PubMed
12.7field-weighted citation impact, top 1% 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

99 citing papers in PubMed, 256 citations in OpenAlex.

  1. Trial
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  8. Induction of immune tolerance in NMOSD and MOGAD.Therapeutic advances in neurological disorders · 2025
    Review
  9. MOG CNS Autoimmunity and MOGAD.Neurology(R) neuroimmunology & neuroinflammation · 2024
    Review
  10. Myelin-reactive B cells exacerbate CD4Nature communications · 2024
    Article
  11. A B cell-driven EAE mouse model reveals the impact of B cell-derived cytokines on CNS autoimmunity.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  12. Review
  13. Visualizing the activation of encephalitogenic T cells in the ileal lamina propria by in vivo two-photon imaging.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  14. Article
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  16. Review
  17. Bcl6 controls meningeal Th17-B cell interaction in murine neuroinflammation.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  18. Article
  19. Article
  20. Article

39 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

7 authors at 3 institutions in 2 countries.

T LitzenburgerMax-Planck-Institut für Neurobiologie, D-82152 Martinsried, Germany.
R Fässler
J Bauer
H Lassmann
C Linington
H Wekerle
A Iglesias
University of Vienna · ATMax Planck Institute of Biochemistry · DEMax Planck Institute of Neurobiology · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We studied the cellular basis of self tolerance of B cells specific for brain autoantigens using transgenic mice engineered to produce high titers of autoantibodies against the myelin oligodendrocyte glycoprotein (MOG), a surface component of central nervous system myelin. We generated "knock-in" mice by replacing the germline JH locus with the rearranged immunoglobulin (Ig) H chain variable (V) gene of a pathogenic MOG-specific monoclonal antibody. In the transgenic mice, conventional B cells reach normal numbers in bone marrow and periphery and express exclusively transgenic H chains, resulting in high titers of MOG-specific serum Igs. Additionally, about one third of transgenic B cells bind MOG, thus demonstrating the absence of active tolerization. Furthermore, peritoneal B-1 lymphocytes are strongly depleted. Upon immunization with MOG, the mature transgenic B cell population undergoes normal differentiation to plasma cells secreting MOG-specific IgG antibodies, during which both Ig isotype switching and somatic mutation occur. In naive transgenic mice, the presence of this substantial autoreactive B cell population is benign, and the mice fail to develop either spontaneous neurological disease or pathological evidence of demyelination. However, the presence of the transgene both accelerates and exacerbates experimental autoimmune encephalitis, irrespective of the identity of the initial autoimmune insult.

Indexed as

Amino Acid SequenceAnimalsAutoantibodiesAutoimmunityB-LymphocytesBrainCell LineCloning, MolecularDisease Models, AnimalEncephalomyelitis, Autoimmune, ExperimentalFlow CytometryGene TargetingImmune ToleranceImmunizationImmunoglobulin GMiceAutoantibodiesImmunoglobulin GMog protein, mouseMyelin-Associated GlycoproteinMyelin-Oligodendrocyte GlycoproteinMyelin Proteins

Identifiers

PMID9653093
PMCPMC2525547
OpenAlexW2029232806

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.