Evidence map›Paper›PMID 24752354›Full record

ArticlePloS one2014

CXCR4 is dispensable for T cell egress from chronically inflamed skin via the afferent lymph.

Skye A Geherin, R Paul Wilson, Silke Jennrich, Gudrun F Debes

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.1field-weighted citation impact, top 25% 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, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. In Sickness and in Health: The Immunological Roles of the Lymphatic System.International journal of molecular sciences · 2021
    Review
  7. Afferent Lymphatic Transport and Peripheral Tissue Immunity.Journal of immunology (Baltimore, Md. : 1950) · 2021
    Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. T Cell Trafficking through Lymphatic Vessels.Frontiers in immunology · 2016
    Review
  16. Effector T Cell Egress via Afferent Lymph Modulates Local Tissue Inflammation.Journal of immunology (Baltimore, Md. : 1950) · 2015
    Article
  17. Lymphatic Regulation of Cellular Trafficking.Journal of clinical & cellular immunology · 2014
    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

4 authors at 1 institution in 1 country.

Skye A GeherinDepartment of Pathobiology, University of Pennsylvania School of Veterinary Medicine, Philadelphia, Pennsylvania, United States of America.
R Paul WilsonDepartment of Pathobiology, University of Pennsylvania School of Veterinary Medicine, Philadelphia, Pennsylvania, United States of America.
Silke JennrichDepartment of Pathobiology, University of Pennsylvania School of Veterinary Medicine, Philadelphia, Pennsylvania, United States of America.
Gudrun F DebesDepartment of Pathobiology, University of Pennsylvania School of Veterinary Medicine, Philadelphia, Pennsylvania, United States of America.
University of Pennsylvania · US

Funding

Regulation of T cell egress from inflamed skinR01AR056730 · NIAMS · UNIVERSITY OF PENNSYLVANIA · PI DEBES, GUDRUN PHILOMENA · 2009 to 2013
$1.7M
Migration of Skin Antibody Secreting CellsF32AR062451 · NIAMS · UNIVERSITY OF PENNSYLVANIA · PI WILSON, RONALD PAUL · 2012 to 2013
$106k
NIAMS NIH HHS F32 AR062451NIAMS NIH HHS F32-AR062451NIAMS NIH HHS R01 AR056730NIAMS NIH HHS R01-AR056730
6 · The paper itself

Abstract

T cell recirculation through extralymphoid tissues is essential to immune surveillance, host defense and inflammation. In this process, T cells enter the tissue from the blood and subsequently leave via the afferent lymph. In the absence of inflammation, T cells require CCR7 expression to egress from the skin or lung, which is consistent with the constitutive expression of the CCR7 ligand CCL21 on lymphatic endothelium. However, during chronic inflammation alternative chemoattractants come into play, allowing Ccr7-deficient (Ccr7-/-) T cells to egress efficiently from affected skin. As T cell egress from inflamed sites is a potential control point of the inflammatory response, we aimed to determine alternative T cell exit receptors using a mouse and a sheep model. We show that CCR7+ and CCR7- T cells exiting from the chronically inflamed skin were highly responsive to the CXCR4 ligand CXCL12, which was induced in the lymphatics in the inflamed site. Based on these findings, we hypothesized that CXCR4 mediates T cell egress from inflamed skin. However, pharmacological inhibition of CXCR4 did not affect the tissue egress of wildtype or Ccr7-/- CD4 and CD8 T cells after adoptive transfer into chronically inflamed skin. Similarly, adoptively transferred Cxcr4-/- Ccr7-/- and Ccr7-/- T cells egressed from the inflamed skin equally well. Based on these data, we conclude that, while CXCR4 might play an essential role for other cell types that enter the afferent lymphatics, it is dispensable for T cell egress from the chronically inflamed skin.

Indexed as

AnimalsChemokine CXCL12ChemotaxisChronic DiseaseHumansInflammationLymphMice, Inbred C57BLReceptors, CCR7Receptors, CXCR4SheepSkinT-LymphocytesCcr7 protein, mouseChemokine CXCL12CXCR4 protein, mouseReceptors, CCR7Receptors, CXCR4

Identifiers

PMID24752354
PMCPMC3994085
OpenAlexW1997788343

What OpenQuestion holds

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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.