Evidence map›Paper›PMID 10880529›Full record

ArticleThe Journal of experimental medicine2000

A B cell superantigen-induced persistent "Hole" in the B-1 repertoire.

G J Silverman, S P Cary, D C Dwyer, L Luo, R Wagenknecht, V E Curtiss

Open access · bronzeAbstract 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 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

28 citing papers in PubMed, 63 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. The molecular characterization of antibody binding to a superantigen-like protein from a commensal microbe.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  5. Article
  6. Immune and Inflammatory Determinants Underlying Alzheimer's Disease Pathology.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2020
    Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Peptidoglycan-linked protein A promotes T cell-dependent antibody expansion during Staphylococcus aureus infection.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. B cell development in GALT: role of bacterial superantigen-like molecules.Journal of immunology (Baltimore, Md. : 1950) · 2010
    Article
  17. Article
  18. Article
  19. Article
  20. Article
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

6 authors at 1 institution in 1 country.

G J SilvermanDepartment of Medicine, University of California at San Diego, La Jolla, California 92093-0663, USA. gsilverman@ucsd.edu
S P Cary
D C Dwyer
L Luo
R Wagenknecht
V E Curtiss
University of California, San Diego · US

Funding

B CELL SUPERANTIGENS AND IMMUNE REGULATIONR01AI040305 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI SILVERMAN, GREGG JOSHUA · 1998 to 2008
$2.4M
VALIDATION OF SELF ADMINISTERED QUALITY OF WELL BEING SCALE IN ARTHRITISP60AR040770 · NIAMS · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI SILVERMAN, GREGG JOSHUA · 1991 to 2000
$787k
ENGINEERED B-CELL SUPERANTIGENS AND IMMUNE TOLERANCER03AI046637 · NIAID · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI SILVERMAN, GREGG JOSHUA · 1999 to 2001
$152k
NIAID NIH HHS AI40305NIAID NIH HHS AI46637NIAID NIH HHS R01 AI040305NIAMS NIH HHS AR40770
6 · The paper itself

Abstract

The bacterial toxin protein A from Staphylococcus aureus (SpA) interacts with B cell antigen receptors encoded by variable region heavy chain (V(H)) clan III genes via a V region framework surface that has been highly conserved during the evolution of the adaptive immune system. We have investigated the consequences of exposure to this prototypic B cell superantigen, and found that treatment of neonates or adults induces a T cell-independent deletion of a large supraclonal set of susceptible B cells that includes clan III/V(H) S107 family-expressing lymphocytes. In studies of different SpA forms, the magnitude of the induced deletion directly correlated with the V(H)-specific binding affinity/avidity. Upon cessation of SpA exposure, the representation of conventional splenic (B-2 subset) lymphocytes normalized; however, we found that the V(H) family-restricted deficit of peritoneal B-1 cells persisted. SpA treatment also induced a persistent loss of splenic S107-mu transcripts, with a loss of certain natural antibodies and specific tolerance to phosphorylcholine immunogens that normally recruit protective antimicrobial responses dominated by the S107-expressing B-1 clone, T15. These studies illustrate how a B cell superantigen can exploit a primordial Achilles heel in the immune system, for which B-1 cells, an important source of natural antibodies and host immune responses, have special susceptibility.

Indexed as

Genes, ImmunoglobulinAdultAnimalsAntibody AffinityB-LymphocytesFlow CytometryHumansImmunoglobulin Heavy ChainsImmunoglobulin Variable RegionInfant, NewbornMiceMice, Inbred BALB CMice, Inbred C57BLReceptors, Antigen, B-CellStaphylococcal Protein ASuperantigensImmunoglobulin Heavy ChainsImmunoglobulin Variable RegionReceptors, Antigen, B-CellStaphylococcal Protein ASuperantigens

Identifiers

PMID10880529
PMCPMC1887708
OpenAlexW2123180572

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.