Evidence map›Paper›PMID 21457936›Full record

ArticleThe American journal of pathology2011

Physiological contribution of CD44 as a ligand for E-Selectin during inflammatory T-cell recruitment.

Maria Nácher, Ana Belén Blázquez, Bojing Shao, Adela Matesanz, Colette Prophete, M Cecilia Berin, Paul S Frenette, Andrés Hidalgo

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.2field-weighted citation impact, top 15% 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

28 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. E-selectin in vascular pathophysiology.Frontiers in immunology · 2024
    Review
  3. Mechanisms Regulating T Cell-Endothelial Cell Interactions.Cold Spring Harbor perspectives in medicine · 2022
    Review
  4. Article
  5. Review
  6. Article
  7. T-Cell Adhesion in Healthy and Inflamed Skin.JID innovations : skin science from molecules to population health · 2021
    Review
  8. The Sweet Smell of Progress With Hyaluronan and Heart Failure.Hypertension (Dallas, Tex. : 1979) · 2021
    Article
  9. Where the Action Is-Leukocyte Recruitment in Atherosclerosis.Frontiers in cardiovascular medicine · 2021
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. 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 4 countries.

Maria NácherDepartment of Epidemiology, Atherothrombosis and Imaging, Centro Nacional de Investigaciones Cardiovasculares, Madrid, Spain.
Ana Belén Blázquez
Bojing Shao
Adela Matesanz
Colette Prophete
M Cecilia Berin
Paul S Frenette
Andrés Hidalgo
Spanish National Centre for Cardiovascular Research · ESIcahn School of Medicine at Mount Sinai · USInstitute of Immunology · HRStem Cell Institute · PAUniversity of Oklahoma Health Sciences Center · US

Funding

In Vivo Sickle Cell Vasoocclusion: Adhesion MechanismsR01HL069438 · NHLBI · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI KELLY, LIBUSHA · 2001 to 2024
$9.5M
NHLBI NIH HHS R01 HL069438NHLBI NIH HHS R01 HL69438
6 · The paper itself

Abstract

Endothelial selectins guide the migration of inflammatory T cells to extralymphoid tissues. Whereas P-selectin glycoprotein ligand-1 (PSGL-1) functions as the exclusive ligand for P-selectin, it acts in coordination with additional glycoproteins to mediate E-selectin binding. CD44 can act as one such ligand in neutrophils, but its contribution in inflammatory T lymphocytes remains unexplored. We have used real-time in vivo imaging of the cremasteric and dermal microcirculations to explore the dynamics of leukocyte recruitment, as well as the physiological contribution of CD44 in a model of Th1-driven inflammation. CD4(+) T-cell rolling frequency and kinetics, as well as arrest, were dependent on endothelial selectins and were markedly altered under inflammatory conditions. CD44 extracted from Th1 cells bound to soluble E-selectin in vitro and cooperated with PSGL-1 by controlling rolling velocities and promoting firm arrest. Using several competitive recruitment assays in a delayed-type hypersensitivity model, we show that the combined absence of CD44 and PSGL-1 impairs inflammatory T-cell recruitment beyond that of PSGL-1 alone. Differential expression of leukocyte fucosyltransferases in these cells may account for the differential use of E-selectin ligands relative to neutrophils. Our results identify additional mechanisms by which CD44 modulates the inflammatory response.

Indexed as

AnimalsCell SeparationChemotaxis, LeukocyteE-SelectinFlow CytometryHyaluronan ReceptorsInflammationLigandsMiceMice, Inbred C57BLReverse Transcriptase Polymerase Chain ReactionTh1 CellsCd44 protein, mouseE-SelectinHyaluronan ReceptorsLigands

Identifiers

PMID21457936
PMCPMC3081198
OpenAlexW1967765380

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.