Evidence map›Paper›PMID 38228717›Full record

ArticleScientific reports2024

Dectin-1 ligands produce distinct training phenotypes in human monocytes through differential activation of signaling networks.

Quen J Cheng, Kylie Farrell, Jeffrey Fenn, Zuchao Ma, Sara K Makanani, Jonathan Siemsen

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

9 citing papers in PubMed, 12 citations in OpenAlex.

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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

6 authors at 2 institutions in 1 country.

Quen J ChengDepartment of Medicine, Division of Infectious Diseases, David Geffen School of Medicine, University of California, Los Angeles, CA, USA. quencheng@ucla.edu.
Kylie FarrellDepartment of Medicine, Division of Infectious Diseases, David Geffen School of Medicine, University of California, Los Angeles, CA, USA.
Jeffrey FennDepartment of Microbiology, Immunology, and Molecular Genetics, University of California, Los Angeles, CA, USA.
Zuchao MaDepartment of Surgery, Center of Excellence in Inflammation, Infectious Disease and Immunity, Quillen College of Medicine, East Tennessee State University, Johnson City, TN, USA.
Sara K MakananiMolecular Biology Institute, University of California, Los Angeles, CA, USA.
Jonathan SiemsenDepartment of Microbiology, Immunology, and Molecular Genetics, University of California, Los Angeles, CA, USA.
University of California, Los Angeles · USEast Tennessee State University · US

Funding

UCLA-CDU CFARP30AI152501 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Grace M Aldrovandi · 2022 to 2026
$15.6M
NFkB dynamics in the stimulus specificity of trained immunityK08AI168567 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Quen J Cheng · 2022 to 2026
$962k
NIAID NIH HHS K08 AI168567NIAID NIH HHS P30 AI152501
6 · The paper itself

Abstract

Cells of the innate immune system retain memory of prior exposures through a process known as innate immune training. β-glucan, a Dectin-1 ligand purified from the Candida albicans cell wall, has been one of the most widely utilized ligands for inducing innate immune training. However, many Dectin-1 ligands exist, and it is not known whether these all produce the same phenotype. Using a well-established in vitro model of innate immune training, we compared two commercially available Dectin-1 agonists, zymosan and depleted zymosan, with the gold standard β-glucan in the literature. We found that depleted zymosan, a β-glucan purified from Saccharomyces cerevisiae cell wall through alkali treatment, produced near identical effects as C. albicans β-glucan. However, untreated zymosan produced a distinct training effect from β-glucans at both the transcript and cytokine level. Training with zymosan diminished, rather than potentiated, induction of cytokines such as TNF and IL-6. Zymosan activated NFκB and AP-1 transcription factors more strongly than β-glucans. The addition of the toll-like receptor (TLR) ligand Pam3CSK4 was sufficient to convert the training effect of β-glucans to a phenotype resembling zymosan. We conclude that differential activation of TLR signaling pathways determines the phenotype of innate immune training induced by Dectin-1 ligands.

Indexed as

beta-GlucansMonocytesCytokinesDectin-1HumansLectins, C-TypeLigandsPhenotypeSaccharomyces cerevisiaeZymosanbeta-GlucansCytokinesDectin-1Lectins, C-TypeLigandsZymosan

Identifiers

PMID38228717
PMCPMC10791629
OpenAlexW4390928843

What OpenQuestion holds

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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.