Evidence map›Paper›PMID 25287444›Full record

ArticleImmunology and cell biology2015

The bullseye synapse formed between CD4+ T-cell and staphylococcal enterotoxin B-pulsed dendritic cell is a suppressive synapse in T-cell response.

Wei Lin, Zhichao Fan, Yuanzhen Suo, Yuting Deng, Min Zhang, Jiyang Wang, Xunbin Wei, Yiwei Chu

Abstract read
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In one paragraph

Article in Immunology and cell biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.2field-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

7 citing papers in PubMed, 11 citations in OpenAlex.

  1. Treg-expressed CTLA-4 depletes CD80/CD86 by trogocytosis, releasing free PD-L1 on antigen-presenting cells.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  2. Visualization of integrin molecules by fluorescence imaging and techniques.Biocell : official journal of the Sociedades Latinoamericanas de Microscopia Electronica ... et. al · 2021
    Article
  3. I-aMediators of inflammation · 2020
    Article
  4. Article
  5. Article
  6. Article
  7. Review
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

8 authors at 5 institutions in 1 country.

Wei Lin1] Department of Immunology and Key Laboratory of Medical Molecular Virology of MOE/MOH, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China [2] Biotherapy Research Centre, Fudan University, Shanghai 200032, China.
Zhichao FanState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai 200030, China.
Yuanzhen SuoState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai 200030, China.
Yuting Deng1] Department of Immunology and Key Laboratory of Medical Molecular Virology of MOE/MOH, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China [2] Biotherapy Research Centre, Fudan University, Shanghai 200032, China.
Min Zhang1] Department of Immunology and Key Laboratory of Medical Molecular Virology of MOE/MOH, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China [2] Biotherapy Research Centre, Fudan University, Shanghai 200032, China.
Jiyang Wang1] Department of Immunology and Key Laboratory of Medical Molecular Virology of MOE/MOH, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China [2] Biotherapy Research Centre, Fudan University, Shanghai 200032, China.
Xunbin WeiState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai 200030, China.
Yiwei Chu1] Department of Immunology and Key Laboratory of Medical Molecular Virology of MOE/MOH, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China [2] Biotherapy Research Centre, Fudan University, Shanghai 200032, China.
Fudan University · CNShanghai Jiao Tong University · CNShanghai Medical College of Fudan University · CNObstetrics and Gynecology Hospital of Fudan University · CNState Key Laboratory of Oncogene and Related Genes · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The immunological synapse (IS) is a supermolecular activation cluster formed between T cells and antigen-presenting cells. Although diverse IS structures have been reported, the function of the IS in T-cell activation remains unclear. Here, we found that the bullseye IS, one of IS types at the interface of CD4(+) T cells and staphylococcal enterotoxin B-pulsed dendritic cells, suppressed CD4(+) T-cell activation, whereas multifocal IS, another synapse type, stimulated CD4(+) T-cell activation. Consistent with these results, bullseye IS formation was accompanied by a low-level calcium response in T cells and a loss of T-cell receptor signalling molecules from the synapse, whereas multifocal IS exhibited the opposite. Furthermore, we found that CD4(+)CD25(+) regulatory T cells (T(regs)) more efficiently formed bullseye IS and promoted bullseye IS formation in CD4(+) CD25(-) T cells. Cytotoxic T-lymphocyte antigen-4 (CTLA-4), an inhibitory molecule expressed continuously on T(regs), was localised in bullseye IS. Moreover, blocking CTLA-4 reduced the percentage of bullseye IS formation and promoted T-cell activation. Our data thus indicate that bullseye IS formation is mediated by CTLA-4, and may negatively control T-cell activation as a suppressive synapse.

Indexed as

AnimalsCalciumCell CommunicationCTLA-4 AntigenDendritic CellsEnterotoxinsFemaleGene Expression RegulationImmunological SynapsesIntercellular Adhesion Molecule-1Lymphocyte ActivationLymphocyte Function-Associated Antigen-1MiceMice, Inbred C57BLProtein BindingReceptors, Antigen, T-CellCalciumCTLA-4 Antigenenterotoxin B, staphylococcalEnterotoxinsIntercellular Adhesion Molecule-1Lymphocyte Function-Associated Antigen-1Receptors, Antigen, T-Cell

Identifiers

PMID25287444
OpenAlexW2092577444

What OpenQuestion holds

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Registered trials

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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.