Evidence map›Paper›PMID 27010197›Full record

ArticlePloS one2016

Integrin-Alpha IIb Identifies Murine Lymph Node Lymphatic Endothelial Cells Responsive to RANKL.

Olga G Cordeiro, Mélanie Chypre, Nathalie Brouard, Simon Rauber, Farouk Alloush, Monica Romera-Hernandez, Cécile Bénézech, Zhi Li, Anita Eckly, Mark C Coles and 7 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

25 citing papers in PubMed, 47 citations in OpenAlex.

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  12. Characterization of CD41Frontiers in immunology · 2022
    Article
  13. Article
  14. Gremlin 1Nature immunology · 2021
    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

17 authors at 8 institutions in 5 countries.

Olga G CordeiroCNRS UPR 3572, University of Strasbourg, Laboratory of Immunopathology and Therapeutic Chemistry/ MEDALIS, Institut de Biologie Moléculaire et Cellulaire, Strasbourg, France.
Mélanie ChypreCNRS UPR 3572, University of Strasbourg, Laboratory of Immunopathology and Therapeutic Chemistry/ MEDALIS, Institut de Biologie Moléculaire et Cellulaire, Strasbourg, France.
Nathalie BrouardINSERM, UMR_S949, Etablissement Français du Sang-Alsace, Faculté de Médecine, Fédération de Médecine Translationnelle, Université de Strasbourg, Strasbourg, France.
Simon RauberCNRS UPR 3572, University of Strasbourg, Laboratory of Immunopathology and Therapeutic Chemistry/ MEDALIS, Institut de Biologie Moléculaire et Cellulaire, Strasbourg, France.
Farouk AlloushCNRS UPR 3572, University of Strasbourg, Laboratory of Immunopathology and Therapeutic Chemistry/ MEDALIS, Institut de Biologie Moléculaire et Cellulaire, Strasbourg, France.
Monica Romera-HernandezDepartment of Hematology, Erasmus University Medical Center, Rotterdam, The Netherlands.
Cécile BénézechBHF Centre for Cardiovascular Science, Queens Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom.
Zhi LiCenter for Immunology and Infection, Department of Biology, University of York, York, United Kingdom.
Anita EcklyINSERM, UMR_S949, Etablissement Français du Sang-Alsace, Faculté de Médecine, Fédération de Médecine Translationnelle, Université de Strasbourg, Strasbourg, France.
Mark C ColesCenter for Immunology and Infection, Department of Biology, University of York, York, United Kingdom.
Antal RotCenter for Immunology and Infection, Department of Biology, University of York, York, United Kingdom.
Hideo YagitaDepartment of Immunology, Juntendo University School of Medicine, Tokyo, 113-8421, Japan.
Catherine LéonINSERM, UMR_S949, Etablissement Français du Sang-Alsace, Faculté de Médecine, Fédération de Médecine Translationnelle, Université de Strasbourg, Strasbourg, France.
Burkhard LudewigInstitute of Immunobiology, Kantonspital St. Gallen, 9007, St. Gallen, Switzerland.
Tom CupedoDepartment of Hematology, Erasmus University Medical Center, Rotterdam, The Netherlands.
François LanzaINSERM, UMR_S949, Etablissement Français du Sang-Alsace, Faculté de Médecine, Fédération de Médecine Translationnelle, Université de Strasbourg, Strasbourg, France.
Christopher G MuellerCNRS UPR 3572, University of Strasbourg, Laboratory of Immunopathology and Therapeutic Chemistry/ MEDALIS, Institut de Biologie Moléculaire et Cellulaire, Strasbourg, France.
Centre National de la Recherche Scientifique · FRInserm · FRUniversity of York · GBErasmus MC · NLUniversité de Strasbourg · FRJuntendo University · JPKantonsspital St. Gallen · CHUniversity of Edinburgh · GB

Funding

Medical Research Council MR/M011542/1
6 · The paper itself

Abstract

Microenvironment and activation signals likely imprint heterogeneity in the lymphatic endothelial cell (LEC) population. Particularly LECs of secondary lymphoid organs are exposed to different cell types and immune stimuli. However, our understanding of the nature of LEC activation signals and their cell source within the secondary lymphoid organ in the steady state remains incomplete. Here we show that integrin alpha 2b (ITGA2b), known to be carried by platelets, megakaryocytes and hematopoietic progenitors, is expressed by a lymph node subset of LECs, residing in medullary, cortical and subcapsular sinuses. In the subcapsular sinus, the floor but not the ceiling layer expresses the integrin, being excluded from ACKR4+ LECs but overlapping with MAdCAM-1 expression. ITGA2b expression increases in response to immunization, raising the possibility that heterogeneous ITGA2b levels reflect variation in exposure to activation signals. We show that alterations of the level of receptor activator of NF-κB ligand (RANKL), by overexpression, neutralization or deletion from stromal marginal reticular cells, affected the proportion of ITGA2b+ LECs. Lymph node LECs but not peripheral LECs express RANK. In addition, we found that lymphotoxin-β receptor signaling likewise regulated the proportion of ITGA2b+ LECs. These findings demonstrate that stromal reticular cells activate LECs via RANKL and support the action of hematopoietic cell-derived lymphotoxin.

Indexed as

AnimalsCells, CulturedEndothelial CellsFibronectinsLymph NodesLymphotoxin-betaMice, Inbred C57BLPlatelet Membrane Glycoprotein IIbRANK LigandSignal TransductionFibronectinsLymphotoxin-betaPlatelet Membrane Glycoprotein IIbRANK LigandTnfsf11 protein, mouse

Identifiers

PMID27010197
PMCPMC4806919
OpenAlexW2332635847

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.