Evidence map›Paper›PMID 32080959›Full record

ArticleEMBO reports2020

Chemokines and galectins form heterodimers to modulate inflammation.

Veit Eckardt, Michelle C Miller, Xavier Blanchet, Rundan Duan, Julian Leberzammer, Johan Duchene, Oliver Soehnlein, Remco Ta Megens, Anna-Kristin Ludwig, Aurelio Dregni and 12 more

Open access · hybridAbstract read
In one paragraph

Article in EMBO reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
5.3field-weighted citation impact, top 3% 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

51 citing papers in PubMed, 84 citations in OpenAlex.

  1. Review
  2. The Role of Galectin-3 in Liver Inflammation and Fibrosis.Journal of inflammation research · 2026
    Review
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  10. Anchoring immunosuppression to inflamed tissue.Nature biomedical engineering · 2023
    Article
  11. Heterodimers Are an Integral Component of Chemokine Signaling Repertoire.International journal of molecular sciences · 2023
    Review
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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

22 authors at 4 institutions in 3 countries.

Veit EckardtFaculty of Medicine, Institute for Cardiovascular Prevention, Ludwig-Maximilians-University, Munich, Germany.
Michelle C MillerDepartment of Biochemistry, Molecular Biology & Biophysics, Health Sciences Center, University of Minnesota, Minneapolis, MN, USA.
Xavier BlanchetFaculty of Medicine, Institute for Cardiovascular Prevention, Ludwig-Maximilians-University, Munich, Germany.
Rundan DuanFaculty of Medicine, Institute for Cardiovascular Prevention, Ludwig-Maximilians-University, Munich, Germany.
Julian LeberzammerFaculty of Medicine, Institute for Cardiovascular Prevention, Ludwig-Maximilians-University, Munich, Germany.
Johan DucheneFaculty of Medicine, Institute for Cardiovascular Prevention, Ludwig-Maximilians-University, Munich, Germany.ORCID 0000-0002-3973-0022
Oliver SoehnleinFaculty of Medicine, Institute for Cardiovascular Prevention, Ludwig-Maximilians-University, Munich, Germany.
Remco Ta MegensFaculty of Medicine, Institute for Cardiovascular Prevention, Ludwig-Maximilians-University, Munich, Germany.
Anna-Kristin LudwigFaculty of Veterinary Medicine, Institute of Physiological Chemistry, Ludwig-Maximilians-University, Munich, Germany.
Aurelio DregniDepartment of Biochemistry, Molecular Biology & Biophysics, Health Sciences Center, University of Minnesota, Minneapolis, MN, USA.
Alexander FaussnerFaculty of Medicine, Institute for Cardiovascular Prevention, Ludwig-Maximilians-University, Munich, Germany.
Kanin WichapongCardiovascular Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands.
Hans IppelCardiovascular Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands.
Ingrid DijkgraafCardiovascular Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands.
Herbert KaltnerFaculty of Veterinary Medicine, Institute of Physiological Chemistry, Ludwig-Maximilians-University, Munich, Germany.
Yvonne DöringFaculty of Medicine, Institute for Cardiovascular Prevention, Ludwig-Maximilians-University, Munich, Germany.
Kiril BidzhekovFaculty of Medicine, Institute for Cardiovascular Prevention, Ludwig-Maximilians-University, Munich, Germany.
Tilman M HackengCardiovascular Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands.
Christian WeberFaculty of Medicine, Institute for Cardiovascular Prevention, Ludwig-Maximilians-University, Munich, Germany.
Hans-Joachim GabiusFaculty of Veterinary Medicine, Institute of Physiological Chemistry, Ludwig-Maximilians-University, Munich, Germany.
Philipp von Hundelshausen *Faculty of Medicine, Institute for Cardiovascular Prevention, Ludwig-Maximilians-University, Munich, Germany.ORCID 0000-0001-7474-9370
Kevin H Mayo *Department of Biochemistry, Molecular Biology & Biophysics, Health Sciences Center, University of Minnesota, Minneapolis, MN, USA.
Ludwig-Maximilians-Universität München · DEMaastricht University · NLUniversity of Minnesota · USGerman Centre for Cardiovascular Research · DE

Funding

Deutsche Forschungsgemeinschaft (DFG) INST 409/150-1 FUGGDeutsche Forschungsgemeinschaft (DFG) SFB1123, A1Deutsche Forschungsgemeinschaft (DFG) sfb1123 A2Deutsche Forschungsgemeinschaft (DFG) SFB1123, B08Deutsche Forschungsgemeinschaft (DFG) SFB1123, Z1Deutsche Forschungsgemeinschaft (DFG) SFB914, B08Minnesota Medical FoundationNational Science Foundation (NSF) BIR-961477University of Minnesota Medical School
6 · The paper itself

Abstract

Chemokines and galectins are simultaneously upregulated and mediate leukocyte recruitment during inflammation. Until now, these effector molecules have been considered to function independently. Here, we tested the hypothesis that they form molecular hybrids. By systematically screening chemokines for their ability to bind galectin-1 and galectin-3, we identified several interacting pairs, such as CXCL12 and galectin-3. Based on NMR and MD studies of the CXCL12/galectin-3 heterodimer, we identified contact sites between CXCL12 β-strand 1 and Gal-3 F-face residues. Mutagenesis of galectin-3 residues involved in heterodimer formation resulted in reduced binding to CXCL12, enabling testing of functional activity comparatively. Galectin-3, but not its mutants, inhibited CXCL12-induced chemotaxis of leukocytes and their recruitment into the mouse peritoneum. Moreover, galectin-3 attenuated CXCL12-stimulated signaling via its receptor CXCR4 in a ternary complex with the chemokine and receptor, consistent with our structural model. This first report of heterodimerization between chemokines and galectins reveals a new type of interaction between inflammatory mediators that can underlie a novel immunoregulatory mechanism in inflammation. Thus, further exploration of the chemokine/galectin interactome is warranted.

Indexed as

GalectinsInflammationAnimalsChemotaxisLeukocytesMiceSignal TransductionGalectinschemotaxisCXCL12galectin-3G protein-coupled receptorlectin

Identifiers

PMID32080959
PMCPMC7132340
OpenAlexW3007057280

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.