Evidence map›Paper›PMID 38661718›Full record

ArticleThe Journal of experimental medicine2024

Dual fluorescence reporter mice for Ccl3 transcription, translation, and intercellular communication.

Maria Belen Rodrigo, Anna De Min, Selina Kathleen Jorch, Cristina Martin-Higueras, Ann-Kathrin Baumgart, Beata Goldyn, Sara Becker, Natalio Garbi, Niels A Lemmermann, Christian Kurts

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.5field-weighted citation impact, top 37% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. 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

10 authors at 2 institutions in 1 country.

Maria Belen RodrigoInstitute of Molecular Medicine and Experimental Immunology, Faculty of Medicine, University Hospital of Bonn University , Bonn, Germany.ORCID 0000-0002-5741-2554
Anna De MinInstitute of Molecular Medicine and Experimental Immunology, Faculty of Medicine, University Hospital of Bonn University , Bonn, Germany.ORCID 0009-0009-9229-6737
Selina Kathleen JorchInstitute of Molecular Medicine and Experimental Immunology, Faculty of Medicine, University Hospital of Bonn University , Bonn, Germany.ORCID 0000-0002-6356-5012
Cristina Martin-HiguerasInstitute of Molecular Medicine and Experimental Immunology, Faculty of Medicine, University Hospital of Bonn University , Bonn, Germany.ORCID 0000-0003-1139-4642
Ann-Kathrin BaumgartInstitute of Molecular Medicine and Experimental Immunology, Faculty of Medicine, University Hospital of Bonn University , Bonn, Germany.ORCID 0000-0002-4763-2588
Beata GoldynInstitute of Molecular Medicine and Experimental Immunology, Faculty of Medicine, University Hospital of Bonn University , Bonn, Germany.ORCID 0000-0002-8858-2660
Sara BeckerInstitute of Virology, Faculty of Medicine, University Hospital of Bonn University , Bonn, Germany.ORCID 0000-0001-5182-2360
Natalio Garbi *Institute of Molecular Medicine and Experimental Immunology, Faculty of Medicine, University Hospital of Bonn University , Bonn, Germany.ORCID 0000-0003-4144-6917
Niels A Lemmermann *Institute of Virology, Faculty of Medicine, University Hospital of Bonn University , Bonn, Germany.ORCID 0000-0001-9190-6497
Christian Kurts *Institute of Molecular Medicine and Experimental Immunology, Faculty of Medicine, University Hospital of Bonn University , Bonn, Germany.ORCID 0000-0002-6620-2401
University Hospital Bonn · DEJohannes Gutenberg University Mainz · DE

Funding

Deutsche Forschungsgemeinschaft 216372401
6 · The paper itself

Abstract

Chemokines guide immune cells during their response against pathogens and tumors. Various techniques exist to determine chemokine production, but none to identify cells that directly sense chemokines in vivo. We have generated CCL3-EASER (ErAse, SEnd, Receive) mice that simultaneously report for Ccl3 transcription and translation, allow identifying Ccl3-sensing cells, and permit inducible deletion of Ccl3-producing cells. We infected these mice with murine cytomegalovirus (mCMV), where Ccl3 and NK cells are critical defense mediators. We found that NK cells transcribed Ccl3 already in homeostasis, but Ccl3 translation required type I interferon signaling in infected organs during early infection. NK cells were both the principal Ccl3 producers and sensors of Ccl3, indicating auto/paracrine communication that amplified NK cell response, and this was essential for the early defense against mCMV. CCL3-EASER mice represent the prototype of a new class of dual fluorescence reporter mice for analyzing cellular communication via chemokines, which may be applied also to other chemokines and disease models.

Indexed as

Cell CommunicationChemokine CCL3Models, AnimalProtein BiosynthesisTranscription, GeneticAnimalsGene Knock-In TechniquesHerpesviridae InfectionsInterferon-betaKiller Cells, NaturalMiceMice, TransgenicMuromegalovirusChemokine CCL3Interferon-beta

Identifiers

PMID38661718
PMCPMC11044946
OpenAlexW4395466400

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.