Evidence map›Paper›PMID 30232280›Full record

ArticleJCI insight2018

Imbalance of immunological synapse-kinapse states reflects tumor escape to immunity in glioblastoma.

Laura R Díaz, Elena Saavedra-López, Leire Romarate, Izaskun Mitxitorena, Paola V Casanova, George P Cribaro, José M Gallego, Ana Pérez-Vallés, Jerónimo Forteza-Vila, Clara Alfaro-Cervello and 3 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 2 pooled it
0.8field-weighted citation impact, top 30% 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, 2 syntheses or guidelines pooled it, 28 citations in OpenAlex.

  1. Pooled it
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  4. Solution structure and synaptic analyses reveal determinants of bispecific T cell engager potency.Proceedings of the National Academy of Sciences of the United States of America · 2025
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  6. SubvertingBiology · 2024
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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

13 authors at 4 institutions in 1 country.

Laura R DíazDepartment of Biochemistry and Molecular Biology, School of Medicine, and.
Elena Saavedra-LópezDepartment of Biochemistry and Molecular Biology, School of Medicine, and.
Leire RomarateDepartment of Biochemistry and Molecular Biology, School of Medicine, and.
Izaskun MitxitorenaDepartment of Biochemistry and Molecular Biology, School of Medicine, and.
Paola V CasanovaDepartment of Biochemistry and Molecular Biology, School of Medicine, and.
George P CribaroDepartment of Biochemistry and Molecular Biology, School of Medicine, and.
José M GallegoDepartment of Neurosurgery and.
Ana Pérez-VallésDepartment of Pathology, Valencia General Hospital, Valencia, Spain.
Jerónimo Forteza-VilaUnidad Mixta CIPF/UCV de Investigación Oncológica, Instituto Valenciano de Patología, Universidad Católica de Valencia, Valencia, Spain.
Clara Alfaro-CervelloLaboratory of Comparative Neurobiology, Instituto Cavanilles, Universitat de València, CIBERNED, Valencia, Spain.
José M García-VerdugoLaboratory of Comparative Neurobiology, Instituto Cavanilles, Universitat de València, CIBERNED, Valencia, Spain.
Carlos BarciaDepartment of Neurosurgery and.
Carlos BarciaDepartment of Biochemistry and Molecular Biology, School of Medicine, and.
Universitat Autònoma de Barcelona · ESUniversitat de València · ESHospital General Universitario De Valencia · ESValencia Catholic University Saint Vincent Martyr · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Since the proper activation of T cells requires the physical interaction with target cells through the formation of immunological synapses (IS), an alteration at this level could be a reason why tumors escape the immune response. As part of their life cycle, it is thought that T cells alternate between a static phase, the IS, and a dynamic phase, the immunological kinapse (IK), depending on high or low antigen sensing. Our investigation performed in tissue samples of human glioma shows that T cells are able to establish synapsing interactions not only with glioma tumorigenic cells, but also with stromal myeloid cells. Particularly, the IS displaying a T cell receptor-rich (TCR-rich) central supramolecular activation cluster (cSMAC) is preferentially established with stromal cells, as opposed to malignant cells. Conversely, T cells in the malignant areas showed distinct morphometric parameters compared with nonneoplastic tissue - the former characterized by an elongated shape, well-suited to kinaptic dynamics. Importantly, high-resolution 3-dimensional analyses demonstrated the existence of bona-fide IK preferentially arranged in malignant areas of the tumor. This imbalance of IS/IK states between these 2 microenvironments reveals the low antigenic sensing of T cells when patrolling tumorigenic cells and reflects the immunoevasive environment of the tumor.

Indexed as

Tumor EscapeAntigen-Presenting CellsBrain NeoplasmsCD3 ComplexGlioblastomaGliomaHumansImaging, Three-DimensionalImmunological SynapsesMyeloid CellsT-LymphocytesTumor MicroenvironmentCD3 ComplexBrain cancerImmunology

Identifiers

PMID30232280
PMCPMC6237222
OpenAlexW2890850037

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.