Evidence map›Paper›PMID 10727464›Full record

ArticleThe Journal of experimental medicine2000

Gene dose-dependent maturation and receptor editing of B cells expressing immunoglobulin (Ig)G1 or IgM/IgG1 tail antigen receptors.

S L Pogue, C C Goodnow

Open access · greenAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

18 citing papers in PubMed, 36 citations in OpenAlex.

  1. IgH isotype-specific B cell receptor expression influences B cell fate.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
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  8. B cell receptor editing in tolerance and autoimmunity.Annals of the New York Academy of Sciences · 2011
    Review
  9. Article
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  11. Maintenance of tolerance by regulation of anti-myeloperoxidase B cells.Journal of the American Society of Nephrology : JASN · 2008
    Article
  12. Article
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  14. Generation of heavy-chain-only antibodies in mice.Proceedings of the National Academy of Sciences of the United States of America · 2006
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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

2 authors at 2 institutions in 2 countries.

S L PogueDepartment of Microbiology and Immunology and Howard Hughes Medical Institute, Stanford University, Palo Alto, California 94305, USA.
C C Goodnow
Australian National University · AUHoward Hughes Medical Institute · US

Funding

MOLECULAR BASIS OF HOST-PARASITE INTERACTIONT32AI007328 · NIAID · STANFORD UNIVERSITY · PI JUSTIN L SONNENBURG · 1987 to 2026
$11.9M
TRANSGENIC MOUSE MODELS FOR B LYMPHOCYTE TOLERANCE AND AUTOIMMUNITYP01AI019512 · NIAID · STANFORD UNIVERSITY · PI MCDEVITT, HUGH O · 1985 to 1998
–
NIAID NIH HHS 5 T32 AI07328NIAID NIH HHS AI19512NIAID NIH HHS T32 AI007328
6 · The paper itself

Abstract

Conserved differences between the transmembrane and cytoplasmic domains of membrane immunoglobulin (Ig)M and IgG may alter the function of antigen receptors on naive versus memory B cells. Here, we compare the ability of these domains to signal B cell allelic exclusion and maturation in transgenic mice. A lysozyme-binding antibody was expressed in parallel sets of mice as IgM, IgG1, or a chimeric receptor with IgM extracellular domains and transmembrane/cytoplasmic domains of IgG1. Like IgM, the IgG1 or chimeric IgM/G receptors triggered heavy chain allelic exclusion and supported development of mature CD21(+) B cells. Many of the IgG or IgM/G B cells became CD21(high) and downregulated their IgG and IgM/G receptors spontaneously, resembling memory B cells and B cells with mutations that exaggerate B cell antigen receptor signaling. Unlike IgM-transgenic mice, "edited" B cells that carry non-hen egg lysozyme binding receptors preferentially accumulated in IgG and IgM/G mice. This was most extreme in lines with the highest transgene copy number and diminished in variant offspring with fewer copies. The sensitivity of B cell maturation to transgene copy number conferred by the IgG transmembrane and cytoplasmic domains may explain the diverse phenotypes found in other IgG-transgenic mouse strains and may reflect exaggerated signaling.

Indexed as

Gene DosageAnimalsB-Lymphocyte SubsetsCell DifferentiationChickensDNA-Binding ProteinsDose-Response Relationship, ImmunologicFemaleGenetic VectorsImmunoglobulin Heavy ChainsImmunoglobulin MMiceMice, Inbred C57BLMice, Inbred CBAMice, TransgenicMuramidaseDNA-Binding ProteinsImmunoglobulin Heavy ChainsImmunoglobulin Mimmunoglobulin M receptorMuramidaseRag2 protein, mouseReceptors, Antigen, B-CellReceptors, FcReceptors, IgGRecombinant Fusion ProteinsTransposasesV(D)J recombination activating protein 2

Identifiers

PMID10727464
PMCPMC2193121
OpenAlexW2100212755

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.