Evidence map›Paper›PMID 32379272›Full record

ArticleThe Journal of experimental medicine2020

The endothelial basement membrane acts as a checkpoint for entry of pathogenic T cells into the brain.

Xueli Zhang, Ying Wang, Jian Song, Hanna Gerwien, Omar Chuquisana, Anna Chashchina, Cornelia Denz, Lydia Sorokin

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

29 citing papers in PubMed, 47 citations in OpenAlex.

  1. Vascular basement membrane laminins modulate functional zonation of cerebral microvessels.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026
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  13. Integrin α3 promotes TScience immunology · 2023
    Article
  14. Article
  15. Article
  16. CNS Pericytes Modulate Local T Cell Infiltration in EAE.International journal of molecular sciences · 2022
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  17. Article
  18. Article
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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

8 authors.

Xueli ZhangInstitute of Physiological Chemistry and Pathobiochemistry, University of Muenster, Muenster, Germany.
Ying WangInstitute of Physiological Chemistry and Pathobiochemistry, University of Muenster, Muenster, Germany.
Jian SongInstitute of Physiological Chemistry and Pathobiochemistry, University of Muenster, Muenster, Germany.
Hanna GerwienInstitute of Physiological Chemistry and Pathobiochemistry, University of Muenster, Muenster, Germany.
Omar ChuquisanaInstitute of Physiological Chemistry and Pathobiochemistry, University of Muenster, Muenster, Germany.
Anna ChashchinaInstitute of Physiological Chemistry and Pathobiochemistry, University of Muenster, Muenster, Germany.
Cornelia DenzCells-in-Motion Cluster of Excellence, University of Muenster, Muenster, Germany.
Lydia SorokinInstitute of Physiological Chemistry and Pathobiochemistry, University of Muenster, Muenster, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The endothelial cell basement membrane (BM) is a barrier to migrating leukocytes and a rich source of signaling molecules that can influence extravasating cells. Using mice lacking the major endothelial BM components, laminin 411 or 511, in murine experimental autoimmune encephalomyelitis (EAE), we show here that loss of endothelial laminin 511 results in enhanced disease severity due to increased T cell infiltration and altered polarization and pathogenicity of infiltrating T cells. In vitro adhesion and migration assays reveal higher binding to laminin 511 than laminin 411 but faster migration across laminin 411. In vivo and in vitro analyses suggest that integrin α6β1- and αvβ1-mediated binding to laminin 511-high sites not only holds T cells at such sites but also limits their differentiation to pathogenic Th17 cells. This highlights the importance of the interface between the endothelial monolayer and the underlying BM for modulation of immune cell phenotype.

Indexed as

AnimalsBasement MembraneBrainCD4-Positive T-LymphocytesCell AdhesionCell DifferentiationCell MovementEncephalomyelitis, Autoimmune, ExperimentalEndothelial CellsIntegrin alpha6beta1LamininMiceReceptors, VitronectinSpinal CordTh17 CellsT-LymphocytesIntegrin alpha6beta1integrin alphavbeta1LamininReceptors, Vitronectin

Identifiers

PMID32379272
PMCPMC7336306
OpenAlexW3022254302

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.