Evidence map›Paper›PMID 27474074›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2016

Leishmania major Infection-Induced VEGF-A/VEGFR-2 Signaling Promotes Lymphangiogenesis That Controls Disease.

Tiffany Weinkopff, Christoph Konradt, David A Christian, Dennis E Discher, Christopher A Hunter, Phillip Scott

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
1.1field-weighted citation impact, top 20% 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

32 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. From defense to disease: the multifaceted role of lymphatics during infection.Journal of immunology (Baltimore, Md. : 1950) · 2025
    Review
  5. Oxygen and immunity toInfection and immunity · 2025
    Review
  6. Article
  7. Lack of Hypoxia Inducible Factor-1α Influences on Macrophages Ability to Deal withJID innovations : skin science from molecules to population health · 2025
    Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Anatomical Vascular Differences andPathogens (Basel, Switzerland) · 2024
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. 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

6 authors at 1 institution in 1 country.

Tiffany WeinkopffDepartment of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104; and.
Christoph KonradtDepartment of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104; and.
David A ChristianDepartment of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104; and.
Dennis E DischerBiophysical Eng'g Labs, University of Pennsylvania, Philadelphia, PA 19104.
Christopher A HunterDepartment of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104; and.
Phillip ScottDepartment of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104; and pscott@vet.upenn.edu.
University of Pennsylvania · US

Funding

PSOC@Penn Education and OutreachU54CA193417 · NCI · UNIVERSITY OF PENNSYLVANIA · PI DISCHER, DENNIS E. · 2015 to 2020
$10.5M
Nanoscience of 'Self' - reductionist approaches to hCD47 inhibition of phagocytesR01HL124106 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI DISCHER, DENNIS E. · 2014 to 2022
$3.1M
Protective and Pathologic Roles for CD8+ T cells in LeishmaniasisR01AI106842 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI SCOTT, PHILLIP · 2014 to 2017
$1.6M
The Role of Myeloid Lineage Cells in LeishmaniasisF32AI114080 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI WEINKOPFF, TIFFANY S · 2014 to 2016
$162k
NCI NIH HHS U54 CA193417NHLBI NIH HHS R01 HL124106NIAID NIH HHS F32 AI114080NIAID NIH HHS R01 AI106842
6 · The paper itself

Abstract

Cutaneous leishmaniasis causes a spectrum of diseases from self-healing to severe nonhealing lesions. Defining the factors contributing to lesion resolution may help in developing new therapies for those patients with chronic disease. We found that infection with Leishmania major increases the expression of vascular endothelial growth factor-A and vascular endothelial growth factor receptor (VEGFR)-2 and is associated with significant changes in the blood and lymphatic vasculature at the site of infection. Ab blockade of VEGFR-2 during infection led to a reduction in lymphatic endothelial cell proliferation and simultaneously increased lesion size without altering the parasite burden. These data show that L. major infection initiates enhanced vascular endothelial growth factor-A/VEGFR-2 signaling and suggest that VEGFR-2-dependent lymphangiogenesis is a mechanism that restricts tissue inflammation in leishmaniasis.

Indexed as

Leishmania majorLymphangiogenesisSignal TransductionAnimalsAntibodiesDermisEndothelial CellsLeishmaniasis, CutaneousLymphatic VesselsMiceMice, Inbred C57BLParasite LoadVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-2AntibodiesVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-2VEGFA protein, human

Identifiers

PMID27474074
PMCPMC5001553
OpenAlexW2475700549

What OpenQuestion holds

Textmetadata
LicenceTDM
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.