Evidence map›Paper›PMID 39044999›Full record

ArticleNature cardiovascular research2024

Identification of a non-canonical chemokine-receptor pathway suppressing regulatory T cells to drive atherosclerosis.

Yvonne Döring, Emiel P C van der Vorst, Yi Yan, Carlos Neideck, Xavier Blanchet, Yvonne Jansen, Manuela Kemmerich, Soyolmaa Bayasgalan, Linsey J F Peters, Michael Hristov and 20 more

Abstract read
In one paragraph

Article in Nature cardiovascular research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

21 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Nanomaterials-Based Immunotherapy for Atherosclerosis.Small (Weinheim an der Bergstrasse, Germany) · 2026
    Review
  4. Monocyte Chemokines Enhance Atherosclerotic Plaque Necrosis After Bacterial Kidney Infection.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Review
  20. Emerging Anti-Inflammatory COPD Treatments: Potential Cardiovascular Impacts.International journal of chronic obstructive pulmonary disease · 2024
    Review
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

30 authors.

Yvonne DöringDivision of Angiology, Swiss Cardiovascular Center, Inselspital, Bern University Hospital, University of Bern, Switzerland.
Emiel P C van der VorstInstitute for Cardiovascular Prevention (IPEK), LMU Munich, Munich, Germany.
Yi YanInstitute for Cardiovascular Prevention (IPEK), LMU Munich, Munich, Germany.
Carlos NeideckInstitute for Cardiovascular Prevention (IPEK), LMU Munich, Munich, Germany.
Xavier BlanchetInstitute for Cardiovascular Prevention (IPEK), LMU Munich, Munich, Germany.
Yvonne JansenInstitute for Cardiovascular Prevention (IPEK), LMU Munich, Munich, Germany.
Manuela KemmerichInstitute for Cardiovascular Prevention (IPEK), LMU Munich, Munich, Germany.
Soyolmaa BayasgalanInstitute for Cardiovascular Prevention (IPEK), LMU Munich, Munich, Germany.
Linsey J F PetersInstitute for Cardiovascular Prevention (IPEK), LMU Munich, Munich, Germany.
Michael HristovInstitute for Cardiovascular Prevention (IPEK), LMU Munich, Munich, Germany.
Kiril BidzhekovInstitute for Cardiovascular Prevention (IPEK), LMU Munich, Munich, Germany.
Changjun YinInstitute for Cardiovascular Prevention (IPEK), LMU Munich, Munich, Germany.
Xi ZhangInstitute for Cardiovascular Prevention (IPEK), LMU Munich, Munich, Germany.
Julian LeberzammerInstitute for Cardiovascular Prevention (IPEK), LMU Munich, Munich, Germany.
Ya LiInstitute for Cardiovascular Prevention (IPEK), LMU Munich, Munich, Germany.
Inhye ParkThe Kennedy Institute of Rheumatology, Nuffield Department of Orthopedics, Rheumatology and Musculoskeletal Sciences, University of Oxford, United Kingdom.
Maria KralInstitute for Cardiovascular Prevention (IPEK), LMU Munich, Munich, Germany.
Katrin NitzInstitute for Cardiovascular Prevention (IPEK), LMU Munich, Munich, Germany.
Laura ParmaInstitute for Cardiovascular Prevention (IPEK), LMU Munich, Munich, Germany.
Selin GencerInstitute for Cardiovascular Prevention (IPEK), LMU Munich, Munich, Germany.
Andreas HabenichtInstitute for Cardiovascular Prevention (IPEK), LMU Munich, Munich, Germany.
Alexander FaussnerInstitute for Cardiovascular Prevention (IPEK), LMU Munich, Munich, Germany.
Daniel TeupserInstitute of Laboratory Medicine, University Hospital, LMU Munich, Germany.
Claudia MonacoMunich Cluster for Systems Neurology (SyNergy), Munich, Germany.
Lesca HoldtInstitute of Laboratory Medicine, University Hospital, LMU Munich, Germany.
Remco T A MegensInstitute for Cardiovascular Prevention (IPEK), LMU Munich, Munich, Germany.
Dorothee AtzlerInstitute for Cardiovascular Prevention (IPEK), LMU Munich, Munich, Germany.
Donato SantovitoInstitute for Cardiovascular Prevention (IPEK), LMU Munich, Munich, Germany.
Philipp von HundelshausenInstitute for Cardiovascular Prevention (IPEK), LMU Munich, Munich, Germany.
Christian WeberInstitute for Cardiovascular Prevention (IPEK), LMU Munich, Munich, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CCL17 is produced by conventional dendritic cells (cDCs), signals through CCR4 on regulatory T cells (Tregs), and drives atherosclerosis by suppressing Treg functions through yet undefined mechanisms. Here we show that cDCs from CCL17-deficient mice display a pro-tolerogenic phenotype and transcriptome that is not phenocopied in mice lacking its cognate receptor CCR4. In the plasma of CCL17-deficient mice, CCL3 was the only decreased cytokine/chemokine. We found that CCL17 signaled through CCR8 as an alternate high-affinity receptor, which induced CCL3 expression and suppressed Treg functions in the absence of CCR4. Genetic ablation of CCL3 and CCR8 in CD4

Indexed as

atherosclerosischemokine receptorschemokinesregulatory T cells

Identifiers

PMID39044999
PMCPMC7616283

What OpenQuestion holds

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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.