Evidence map›Paper›PMID 11012771›Full record

ArticleImmunology2000

Staphylococcal enterotoxin B induces potent cytotoxic activity by intraepithelial lymphocytes.

A I Roberts, R S Blumberg, A D Christ, R E Brolin, E C Ebert

Open access · greenAbstract read
In one paragraph

Article in Immunology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.7field-weighted citation impact, top 33% 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

8 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. Role of HLA typing on Crohn's disease pathogenesis.Annals of medicine and surgery (2012) · 2015
    Article
  3. Review
  4. Article
  5. Article
  6. Staphylococcal enterocolitis: forgotten but not gone?Digestive diseases and sciences · 2010
    Review
  7. Article
  8. 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

5 authors at 2 institutions in 1 country.

A I RobertsDepartment of Medicine, UMDNJ-Robert Wood Johnson Medical School, New Brunswick, NJ 08903, USA.
R S Blumberg
A D Christ
R E Brolin
E C Ebert
Harvard University · USJohnson University · US

Funding

Regulation of Mucosal LymphocytesR01DK051362 · NIDDK · BRIGHAM AND WOMEN'S HOSPITAL · PI Richard S Blumberg, Yu-Hwa Huang Blumberg · 1997 to 2026
$13.5M
MOLECULAR CHARACTERIZATION OF MUCOSAL LYMPHOCYTESR01DK044319 · NIDDK · BRIGHAM AND WOMEN'S HOSPITAL · PI Richard S Blumberg · 1992 to 2026
$10.4M
Characterization of Mucosal LymphocytesR37DK044319 · NIDDK · BRIGHAM AND WOMEN'S HOSPITAL · PI BLUMBERG, RICHARD S · 2005 to 2014
$7.2M
INTRAEPITHELIAL LYMPHOCYTES RELATION TO EPITHELIAL CELLSR01DK042166 · NIDDK · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI EBERT, ELLEN CATHERINE · 1990 to 2002
$654k
NIDDK NIH HHS DK42166NIDDK NIH HHS DK44319NIDDK NIH HHS DK51362NIDDK NIH HHS R01 DK044319NIDDK NIH HHS R01 DK051362NIDDK NIH HHS R37 DK044319
6 · The paper itself

Abstract

In food poisoning, Staphylococcus aureus secretes staphylococcal enterotoxin B (SEB), a superantigen that causes intense T-cell proliferation and cytotoxicity. The effects of SEB on lytic activity by human intestinal intraepithelial lymphocytes (IEL) were investigated. Jejunal IEL, from morbidly obese individuals undergoing gastric bypass operations, were tested for SEB-induced cytotoxicity against C1R B-lymphoblastoid cells, HT-29 adenocarcinoma cells, or CD1d-transfected cells using the 51Cr-release assay. Fas and Fas ligand expression were detected by immunofluorescence and flow cytometry and soluble ligand by enzyme-linked immunosorbent assay (ELISA). In the presence of SEB, IEL became potently cytotoxic against C1R cells and interferon-gamma (IFN-gamma)-precultured HT-29 cells, causing 55+/-10% and 31+/-6% lysis, respectively, greater than that by phytohaemagglutinin (PHA)-, interleukin-2 (IL-2)-, or anti-T-cell receptor (TCR)-activated IEL. SEB-stimulated peripheral blood (PB) CD8+ T cells lysed similar numbers of C1R cells but fewer HT-29 cells (53+/-13% and 8+/-5%, respectively). IEL killing of C1R cells involved interaction of major histocompatibility complex (MHC) class II with TCR, CD2 with CD58, and CD11a with CD54, and was perforin mediated. SEB-induced IEL lysis of HT-29 cells, in contrast, was caused by an unknown target cell structure, not MHC class II or CD1d, and resulted from a combination of perforin and Fas-mediated events. The potent cytotoxic activities of IEL promoted by SEB utilize two different mechanisms, depending on the surface receptors expressed by the target cells.

Indexed as

Antigens, CD1Antigens, CD1dCD8-Positive T-LymphocytesCell Culture TechniquesCytotoxicity, ImmunologicEnterotoxinsEpithelial Cellsfas ReceptorHumansIntestinal MucosaJejunumStaphylococcus aureusSuperantigensTumor Cells, CulturedAntigens, CD1Antigens, CD1dCD1D protein, humanenterotoxin B, staphylococcalEnterotoxinsfas ReceptorSuperantigens

Identifiers

PMID11012771
PMCPMC2327067
OpenAlexW2057591378

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.