Evidence map›Paper›PMID 10477549›Full record

ArticleThe Journal of experimental medicine1999

Autoantigen-specific B cell activation in Fas-deficient rheumatoid factor immunoglobulin transgenic mice.

H Wang, M J Shlomchik

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

24 citing papers in PubMed, 73 citations in OpenAlex.

  1. Article
  2. Glucose Requirement of Antigen-Specific Autoreactive B Cells and CD4+ T Cells.Journal of immunology (Baltimore, Md. : 1950) · 2023
    Article
  3. Review
  4. Article
  5. Article
  6. Requirement for Transcription Factor Ets1 in B Cell Tolerance to Self-Antigens.Journal of immunology (Baltimore, Md. : 1950) · 2015
    Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Murine B cell response to TLR7 ligands depends on an IFN-beta feedback loop.Journal of immunology (Baltimore, Md. : 1950) · 2009
    Article
  14. B cells and immunological tolerance.The Journal of investigative dermatology · 2009
    Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review
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

2 authors at 1 institution in 1 country.

H WangDepartment of Laboratory Medicine, Yale University School of Medicine, New Haven, Connecticut 06520-8035, USA.
M J Shlomchik
Yale University · US

Funding

TOLERANCE AND AUTOIMMUNITY IN RF TRANSGENIC MICEP01AI036529 · NIAID · YALE UNIVERSITY · PI FLAVELL, RICHARD A · 1994 to 2006
$9.4M
NIAID NIH HHS P01 AI036529NIAID NIH HHS P01 AI36529
6 · The paper itself

Abstract

In systemic autoimmune disease, self-tolerance fails, leading to autoantibody production. A central issue in immunology is to understand the origins of activated self-reactive B cells. We have used immunoglobulin (Ig) transgenic mice to investigate the regulation of autoreactive B cells with specificity for self-IgG2a (the rheumatoid factor [RF] specificity) to understand how normal mice regulate RF autoantibodies and how this fails in autoimmune mice. We previously showed that normal mice do not tolerize the AM14 RF clone, nor do they appear to activate it. Here we show that in Fas-deficient autoimmune mice, the picture is quite different. RF B cells are activated to divide and secrete, but only when the autoantigen is present. Thus, B cells that are ignored rather than anergized in normal mice can be stimulated to produce autoantibody in Fas-deficient mice. This demonstrates a novel developmental step at which intact Fas-Fas ligand signaling is required to regulate B cells in order to prevent autoimmunity. These data also establish the relevance of ignorant self-specific B cells to autoantibody production in disease and prove that in the case of the RF specificity, the nominal autoantigen IgG2a is the driving autoantigen in vivo.

Indexed as

AutoantigensAnimalsAutoantibodiesAutoimmune DiseasesAutoimmunityB-Lymphocytesfas ReceptorImmunoglobulin GImmunoglobulin Heavy ChainsLymphocyte ActivationLymphocyte CountMiceMice, Inbred BALB CMice, TransgenicRheumatoid FactorSelf ToleranceAutoantibodiesAutoantigensfas ReceptorImmunoglobulin GImmunoglobulin Heavy ChainsRheumatoid Factor

Identifiers

PMID10477549
PMCPMC2195612
OpenAlexW2139775368

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.