Evidence map›Paper›PMID 10816471›Full record

ArticleInfection and immunity2000

Inhibition of staphylococcal enterotoxin B-induced lymphocyte proliferation and tumor necrosis factor alpha secretion by MAb5, an anti-toxic shock syndrome toxin 1 monoclonal antibody.

L T Pang, W W Kum, A W Chow

Abstract read
In one paragraph

Article in Infection and immunity, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

17 citing papers in PubMed, 34 citations in OpenAlex.

  1. Monoclonal Antibodies Targeting Bacterial Infections: A Broad Review of the Field.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2026
    Review
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  5. Review
  6. Sepsis: mechanisms of bacterial injury to the patient.Scandinavian journal of trauma, resuscitation and emergency medicine · 2019
    Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Heterogeneity of the humoral immune response following Staphylococcus aureus bacteremia.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2010
    Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. 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

3 authors at 2 institutions in 2 countries.

L T PangDepartments of Medicine, University of British Columbia, and Canadian Bacterial Diseases Network and Vancouver Hospital Health Sciences Centre, Vancouver, British Columbia, Canada.
W W Kum
A W Chow
Vancouver Hospital and Health Sciences Centre · CAUniversity of British Columbia · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Toxic shock syndrome (TSS) is primarily caused by toxic shock syndrome toxin-1 (TSST-1) and staphylococcal enterotoxin B (SEB). These toxins belong to a family of pyrogenic toxin superantigens (PTSAgs) produced by Staphylococcus aureus and exhibit several shared biological properties, including the induction of massive cytokine release and Vbeta-specific T-cell proliferation. The crystal structures of most PTSAgs are now published, and they demonstrate a striking similarity in conformational architecture even though their primary protein sequences are different. Despite these structural and immunobiological similarities, no cross-reactivity between TSST-1 and other PTSAgs has been demonstrated in serological or neutralization assays. Our laboratory has developed a neutralizing murine anti-TSST-1 monoclonal antibody (MAb5) which displayed cross-reactivity with SEB by enzyme-linked immunosorbent assay. The aim of the present study was to evaluate whether MAb5 can also cross-neutralize SEB-induced superantigenic activities in vitro. MAb5 was found to partially inhibit SEB-induced T-cell mitogenesis (63%) and tumor necrosis factor alpha (TNF-alpha) secretion (70%) in human peripheral blood mononuclear cells (PBMC) in a dose-dependent manner, while an isotypic anti-TSST-1 monoclonal antibody showed no effect. Epitope mapping revealed that MAb5 bound to TSST-1 residues 47 to 56 ((47)FPSPYYSPAF(56)) and to SEB residues 83 to 92 ((83)DVFGANYYYQ(92)), sequences that located in different regions of these toxins and are structurally dissimilar. SEB peptide (83)DVFGANYYYQ(92) was synthesized and found to also inhibit SEB-induced mitogenesis and TNF-alpha secretion in human PBMC. Our results demonstrate for the first time that MAb5 binds to different epitopes on TSST-1 and SEB that appear functionally important in inducing T-cell mitogenesis and TNF-alpha secretion in vitro.

Indexed as

Bacterial ToxinsAntibodies, BacterialAntibodies, MonoclonalAntibody SpecificityAntigen-Antibody ReactionsBinding SitesCross ReactionsEnterotoxinsEpitope MappingHumansLymphocyte ActivationModels, MolecularShock, SepticSuperantigensTumor Necrosis Factor-alphaAntibodies, BacterialAntibodies, MonoclonalBacterial Toxinsenterotoxin B, staphylococcalenterotoxin F, StaphylococcalEnterotoxinsSuperantigensTumor Necrosis Factor-alpha

Identifiers

PMID10816471
PMCPMC97575
OpenAlexW1991084507

What OpenQuestion holds

Textmetadata
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.