Evidence map›Paper›PMID 39273210›Full record

ArticleInternational journal of molecular sciences2024

Endothelial Cell-Derived Soluble CD200 Determines the Ability of Immune Cells to Cross the Blood-Brain Barrier.

Myriam Pujol, Tautvydas Paskevicius, Alison Robinson, Simran Dhillon, Paul Eggleton, Alex S Ferecskó, Nick Gutowski, Janet Holley, Miranda Smallwood, Jia Newcombe and 2 more

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. 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

12 authors.

Myriam PujolDepartment of Biochemistry, University of Alberta, Edmonton, AB T6G 2H7, Canada.ORCID 0000-0003-1833-3746
Tautvydas PaskeviciusDepartment of Biochemistry, University of Alberta, Edmonton, AB T6G 2H7, Canada.
Alison RobinsonDepartment of Biochemistry, University of Alberta, Edmonton, AB T6G 2H7, Canada.
Simran DhillonDepartment of Biochemistry, University of Alberta, Edmonton, AB T6G 2H7, Canada.
Paul EggletonRevolo Biotherapeutics, Gaithersburg, MD 20878, USA.ORCID 0000-0001-8244-2125
Alex S FerecskóUniversity of Exeter Medical School, University of Exeter, Exeter EX1 2HZ, UK.
Nick GutowskiUniversity of Exeter Medical School, University of Exeter, Exeter EX1 2HZ, UK.
Janet HolleyUniversity of Exeter Medical School, University of Exeter, Exeter EX1 2HZ, UK.
Miranda SmallwoodUniversity of Exeter Medical School, University of Exeter, Exeter EX1 2HZ, UK.ORCID 0000-0001-5526-700X
Jia NewcombeNeuroResource, Department of Neuroinflammation, UCL Queen Square Institute of Neurology, University College London, London WC1E 6BT, UK.
Luis B AgellonSchool of Human Nutrition, McGill University, Sainte Anne de Bellevue, QC H9X 3V9, Canada.ORCID 0000-0002-2209-8702
Marek MichalakDepartment of Biochemistry, University of Alberta, Edmonton, AB T6G 2H7, Canada.

Funding

Canadian Institutes of Health Reserch PS 168843
6 · The paper itself

Abstract

The infiltration of immune cells into the central nervous system mediates the development of autoimmune neuroinflammatory diseases. We previously showed that the loss of either Fabp5 or calnexin causes resistance to the induction of experimental autoimmune encephalomyelitis (EAE) in mice, an animal model of multiple sclerosis (MS). Here we show that brain endothelial cells lacking either Fabp5 or calnexin have an increased abundance of cell surface CD200 and soluble CD200 (sCD200) as well as decreased T-cell adhesion. In a tissue culture model of the blood-brain barrier, antagonizing the interaction of CD200 and sCD200 with T-cell CD200 receptor (CD200R1) via anti-CD200 blocking antibodies or the RNAi-mediated inhibition of CD200 production by endothelial cells increased T-cell adhesion and transmigration across monolayers of endothelial cells. Our findings demonstrate that sCD200 produced by brain endothelial cells regulates immune cell trafficking through the blood-brain barrier and is primarily responsible for preventing activated T-cells from entering the brain.

Indexed as

Antigens, CDBlood-Brain BarrierCell AdhesionEndothelial CellsT-LymphocytesAnimalsBrainEncephalomyelitis, Autoimmune, ExperimentalHumansMiceMice, Inbred C57BLAntigens, CDantigens, CD200brain endothelial cellscalnexinCD200CD200R1fatty acid binding protein 5neurodegenerative diseasessCD200

Identifiers

PMID39273210
PMCPMC11395061

What OpenQuestion holds

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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.