Evidence map›Paper›PMID 31572401›Full record

ArticleFrontiers in immunology2019

Neuropilin-1 Acts as a Receptor for Complement Split Products.

Claire Battin, Annika De Sousa Linhares, Wolfgang Paster, David E Isenman, Markus Wahrmann, Judith Leitner, Gerhard J Zlabinger, Peter Steinberger, Johannes Hofer

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

10 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. C4d, a high-affinity LilrB2 ligand, is elevated in Alzheimer's disease and mediates synapse pruning.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. A widespread viral entry mechanism: The C-end Rule motif-neuropilin receptor interaction.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Review
  9. Review
  10. 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

9 authors at 2 institutions in 2 countries.

Claire BattinDivision of Immune Receptors and T Cell Activation, Center for Pathophysiology, Infectiology, and Immunology, Institute of Immunology, Medical University of Vienna, Vienna, Austria.
Annika De Sousa LinharesDivision of Immune Receptors and T Cell Activation, Center for Pathophysiology, Infectiology, and Immunology, Institute of Immunology, Medical University of Vienna, Vienna, Austria.
Wolfgang PasterDivision of Immune Receptors and T Cell Activation, Center for Pathophysiology, Infectiology, and Immunology, Institute of Immunology, Medical University of Vienna, Vienna, Austria.
David E IsenmanDepartments of Biochemistry and Immunology, University of Toronto, Toronto, ON, Canada.
Markus WahrmannDivision of Nephrology and Dialysis, Department of Internal Medicine III, Medical University Vienna, Vienna, Austria.
Judith LeitnerDivision of Immune Receptors and T Cell Activation, Center for Pathophysiology, Infectiology, and Immunology, Institute of Immunology, Medical University of Vienna, Vienna, Austria.
Gerhard J ZlabingerDivision of Clinical and Experimental Immunology, Center for Pathophysiology, Infectiology, and Immunology, Institute of Immunology, Medical University of Vienna, Vienna, Austria.
Peter SteinbergerDivision of Immune Receptors and T Cell Activation, Center for Pathophysiology, Infectiology, and Immunology, Institute of Immunology, Medical University of Vienna, Vienna, Austria.
Johannes HoferDivision of Nephrology and Dialysis, Department of Internal Medicine III, Medical University Vienna, Vienna, Austria.
Medical University of Vienna · ATUniversity of Toronto · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Complement split products (CSPs), such as the fragments C4d and C3d, which are generated as a consequence of complement regulatory processes, are established markers for disease activity in autoimmunity or antibody-mediated graft rejection. Since immunoglobulin-like transcript 4 (ILT4) was previously shown to interact with soluble CSPs, but not with CSPs covalently-bound to target surfaces following classical complement activation, the present study aimed to identify novel cellular receptors interacting with covalently-deposited CSPs. By applying an unbiased screening approach using a cDNA mammalian expression library generated from human monocyte-derived dendritic cells and probed with recombinant human C4d, we identified neuropilin-1 (NRP1) as a novel receptor for C4d, C3d, and iC3b. NRP1, a highly conserved type 1 transmembrane protein, plays important roles in the development of the nervous and cardiovascular system as well as in tumorigenesis through interaction with its established binding partners, such as vascular endothelial growth factor (VEGF) and semaphorin 3A (Sema3A). NRP1 is also expressed on immune cells and serves as a marker for murine Tregs. Although NRP1 contains domains homologous to ones found in some complement proteins, it has not been linked to the complement system. We demonstrate that binding of C4d to NRP1 expressing cells was dose-dependent and saturable, and had a K

Indexed as

AnimalsCell Line, TumorComplement ActivationComplement C3bComplement C3dComplement C4bComplement System ProteinsHumansJurkat CellsMiceNeuropilin-1Peptide FragmentsProtein BindingReceptors, ComplementSemaphorin-3AVascular Endothelial Growth Factor AComplement C3bComplement C3dComplement C4bcomplement C4dComplement System ProteinsNeuropilin-1Peptide FragmentsReceptors, ComplementSemaphorin-3AVascular Endothelial Growth Factor AC3dC4dcomplement receptorscomplement split productsiC3bneuropilin-1

Identifiers

PMID31572401
PMCPMC6753332
OpenAlexW2971813790

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.