Evidence map›Paper›PMID 32301538›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2020

In response to complement anaphylatoxin peptides C3a and C5a, human vascular endothelial cells migrate and mediate the activation of B-cells and polarization of T-cells.

Pooja Shivshankar, Yi-Dong Li, Stacey L Mueller-Ortiz, Rick A Wetsel

Open access · greenAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.3field-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

30 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Observational
  3. Review
  4. Review
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  6. Article
  7. Review
  8. The Complement System.Advances in experimental medicine and biology · 2025
    Review
  9. Review
  10. Review
  11. Review
  12. Immunity and Coagulation in COVID-19.International journal of molecular sciences · 2024
    Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Review
  18. 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

4 authors at 1 institution in 1 country.

Pooja ShivshankarResearch Center for Immunology and Autoimmune Diseases, Brown Foundation Institute of Molecular Medicine, McGovern Medical School, University of Texas Health Science Center, Houston, TX, USA.
Yi-Dong LiResearch Center for Immunology and Autoimmune Diseases, Brown Foundation Institute of Molecular Medicine, McGovern Medical School, University of Texas Health Science Center, Houston, TX, USA.
Stacey L Mueller-OrtizResearch Center for Immunology and Autoimmune Diseases, Brown Foundation Institute of Molecular Medicine, McGovern Medical School, University of Texas Health Science Center, Houston, TX, USA.
Rick A WetselResearch Center for Immunology and Autoimmune Diseases, Brown Foundation Institute of Molecular Medicine, McGovern Medical School, University of Texas Health Science Center, Houston, TX, USA.
Brown Foundation · US

Funding

MURINE COMPLEMENT C5 DEFICIENCY--MOLECULAR BASISR01AI025011 · NIAID · WASHINGTON UNIVERSITY · PI WETSEL, RICK A. · 1987 to 2017
$4.6M
NIAID NIH HHS R01 AI025011
6 · The paper itself

Abstract

The vascular endothelium has been discovered in the past several years to be important in shaping the cellular immune response. During the immune response the vascular endothelium is constantly perturbed by biologically potent molecules, including the complement activation peptides, C3a and C5a. Despite the importance of C3a and C5a in inflammation and immunity, their role in modulating lymphocyte function via activation of vascular endothelial cells is unknown. Accordingly, we investigated the regulated expression of the C3a and C5a receptors (complement anaphylatoxin C3a receptor [C3aR] and complement anaphylatoxin C5a receptor 1 [C5aR1]) on human umbilical vascular endothelial cells (HUVECs) and examined how C3a or C5a activation of HUVECs affects the activation and polarization of lymphatic cells. Our findings demonstrated that C3a and C5a increase C3aR and C5aR1 expression by HUVECs as well as directing their cellular transmigration and spreading through transwell filters. Moreover, C3a- or C5a-stimulated endothelial cells: (1) caused activation of B-lymphoblasts with significant increase in Fas Ligand (CD95L) (FasL), CD69, and IL-R1 expression, and (2) skewed T-lymphoblast cells toward a Th1 subtype, (CD4

Indexed as

AnaphylatoxinsB-LymphocytesCells, CulturedComplement ActivationComplement C3aComplement C5aEndothelium, VascularHumansHuman Umbilical Vein Endothelial CellsInflammationPeptidesReceptor, Anaphylatoxin C5aReceptors, ComplementSignal TransductionT-LymphocytesAnaphylatoxinsComplement C3acomplement C3a receptorComplement C5aPeptidesReceptor, Anaphylatoxin C5aReceptors, ComplementB-cell and T-cellsC3a and C5aC3aR and C5aR1complementlymphocyte endothelial interactionvascular endothelial cells

Identifiers

PMID32301538
PMCPMC11905332
OpenAlexW3017097384

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.