Evidence map›Paper›PMID 34489975›Full record

ArticleFrontiers in immunology2021

Binding of Staphylococcal Enterotoxin B (SEB) to B7 Receptors Triggers TCR- and CD28-Mediated Inflammatory Signals in the Absence of MHC Class II Molecules.

Martina Kunkl, Carola Amormino, Silvana Caristi, Valentina Tedeschi, Maria Teresa Fiorillo, Revital Levy, Andrey Popugailo, Raymond Kaempfer, Loretta Tuosto

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

19 citing papers in PubMed, 22 citations in OpenAlex.

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  13. A Higher Dose ofToxins · 2023
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  16. Oral exposure toFrontiers in immunology · 2023
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  17. Article
  18. SARS-CoV-2-Specific Immune Response and the Pathogenesis of COVID-19.International journal of molecular sciences · 2022
    Review
  19. Frontiers in immunology · 2022
    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

9 authors at 2 institutions in 1 country.

Martina KunklDepartment of Biology and Biotechnology Charles Darwin, Sapienza University, Rome, Italy.
Carola AmorminoDepartment of Biology and Biotechnology Charles Darwin, Sapienza University, Rome, Italy.
Silvana CaristiDepartment of Biology and Biotechnology Charles Darwin, Sapienza University, Rome, Italy.
Valentina TedeschiDepartment of Biology and Biotechnology Charles Darwin, Sapienza University, Rome, Italy.
Maria Teresa FiorilloDepartment of Biology and Biotechnology Charles Darwin, Sapienza University, Rome, Italy.
Revital LevyDepartment of Biochemistry and Molecular Biology, The Institute for Medical Research Israel-Canada, The Hebrew University-Hadassah Medical School, Jerusalem, Israel.
Andrey PopugailoDepartment of Biochemistry and Molecular Biology, The Institute for Medical Research Israel-Canada, The Hebrew University-Hadassah Medical School, Jerusalem, Israel.
Raymond KaempferDepartment of Biochemistry and Molecular Biology, The Institute for Medical Research Israel-Canada, The Hebrew University-Hadassah Medical School, Jerusalem, Israel.
Loretta TuostoDepartment of Biology and Biotechnology Charles Darwin, Sapienza University, Rome, Italy.
Sapienza University of Rome · ITIstituto Pasteur · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The inflammatory activity of staphylococcal enterotoxin B (SEB) relies on its capacity to trigger polyclonal T-cell activation by binding both T-cell receptor (TCR) and costimulatory receptor CD28 on T cells and MHC class II and B7 molecules on antigen presenting cells (APC). Previous studies highlighted that SEB may bind TCR and CD28 molecules independently of MHC class II, yet the relative contribution of these interactions to the pro-inflammatory function of SEB remained unclear. Here, we show that binding to MHC class II is dispensable for the inflammatory activity of SEB, whereas binding to TCR, CD28 and B7 molecules is pivotal, in both human primary T cells and Jurkat T cell lines. In particular, our finding is that binding of SEB to B7 molecules suffices to trigger both TCR- and CD28-mediated inflammatory signalling. We also provide evidence that, by strengthening the interaction between CD28 and B7, SEB favours the recruitment of the TCR into the immunological synapse, thus inducing lethal inflammatory signalling.

Indexed as

Antigen-Presenting CellsCD28 AntigensCell CommunicationCells, CulturedEnterotoxinsHistocompatibility Antigens Class IIHumansLymphocyte ActivationReceptors, Antigen, T-CellSignal TransductionT-LymphocytesCD28 Antigensenterotoxin B, staphylococcalEnterotoxinsHistocompatibility Antigens Class IIReceptors, Antigen, T-CellCD28inflammatory responsestaphylococcal enterotoxinsT cellsTCR - T cell receptor

Identifiers

PMID34489975
PMCPMC8418141
OpenAlexW3195338211

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.