Evidence map›Paper›PMID 42760443›Full record

ArticleEMBO reports2026

Coenzyme A activates TLR4 and enhances alternative macrophage activation in line with MyD88 agonism.

Anthony E Jones, Amy Rios, Neira Ibrahimovic, Andréa B Ball, Carolina Chavez, Nicholas A Bayley, Natalie A Falta, Marisa Mekkittikul, Clarissa Carrillo, Wei Yuan Hsieh and 8 more

Abstract read
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In one paragraph

Article in EMBO reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

18 authors.

Anthony E JonesDepartments of Molecular and Medical Pharmacology, University of California, Los Angeles, CA, 90095, USA.ORCID http://orcid.org/0000-0003-2058-6021
Amy RiosDepartments of Molecular and Medical Pharmacology, University of California, Los Angeles, CA, 90095, USA.
Neira IbrahimovicDepartments of Molecular and Medical Pharmacology, University of California, Los Angeles, CA, 90095, USA.
Andréa B BallDepartments of Molecular and Medical Pharmacology, University of California, Los Angeles, CA, 90095, USA.ORCID http://orcid.org/0000-0002-8214-7190
Carolina ChavezDepartments of Molecular and Medical Pharmacology, University of California, Los Angeles, CA, 90095, USA.
Nicholas A BayleyDepartments of Molecular and Medical Pharmacology, University of California, Los Angeles, CA, 90095, USA.ORCID http://orcid.org/0000-0003-0489-0592
Natalie A FaltaDepartments of Molecular and Medical Pharmacology, University of California, Los Angeles, CA, 90095, USA.ORCID http://orcid.org/0009-0004-7413-4527
Marisa MekkittikulDepartments of Molecular and Medical Pharmacology, University of California, Los Angeles, CA, 90095, USA.
Clarissa CarrilloDepartments of Molecular and Medical Pharmacology, University of California, Los Angeles, CA, 90095, USA.ORCID http://orcid.org/0009-0006-8786-6406
Wei Yuan HsiehMicrobiology, Immunology, and Molecular Genetics, University of California, Los Angeles, CA, 90095, USA.
Alessandro SammarcoMicrobiology, Immunology, and Molecular Genetics, University of California, Los Angeles, CA, 90095, USA.
Amber B ReyesDepartments of Molecular and Medical Pharmacology, University of California, Los Angeles, CA, 90095, USA.
Angel A CortezDepartments of Molecular and Medical Pharmacology, University of California, Los Angeles, CA, 90095, USA.
Thomas G GraeberDepartments of Molecular and Medical Pharmacology, University of California, Los Angeles, CA, 90095, USA.ORCID http://orcid.org/0000-0001-8574-9181
Richard L WatsonMedicine, Division of Pulmonary and Critical Care Medicine; University of California, Los Angeles, CA, 90095, USA.
Alexander HoffmannMicrobiology, Immunology, and Molecular Genetics, University of California, Los Angeles, CA, 90095, USA.
Steven J BensingerMicrobiology, Immunology, and Molecular Genetics, University of California, Los Angeles, CA, 90095, USA.ORCID http://orcid.org/0000-0002-9657-4206
Ajit S DivakaruniDepartments of Molecular and Medical Pharmacology, University of California, Los Angeles, CA, 90095, USA. adivakaruni@mednet.ucla.edu.ORCID http://orcid.org/0000-0002-2528-9651

Funding

Understanding the Influence of Lipid Homeostasis on T cell FunctionP01HL146358 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI YOUNG, STEPHEN G. · 2019 to 2023
$11.7M
TUMOR CELL SURFACES AND CHROMOSOMEST32CA009056 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Gay M Crooks, David A. Nathanson · 1985 to 2026
$10.5M
Characterizing functional states of macrophages via their stimulus-responsesR01AI173214 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Alexander Hoffmann · 2023 to 2026
$2.8M
Understanding How Metabolic Cofactors Control Cell Function and FateR35GM138003 · NIGMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Ajit Divakaruni · 2020 to 2026
$2.8M
Chemistry Biology Interface Training ProgramT32GM136614 · NIGMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Patrick G. Harran · 2020 to 2026
$2.8M
Investigating the impact of a fatty acid-cRel inflammatory circuit in atherosclerosisR01HL157710 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BENSINGER, STEVEN J · 2021 to 2024
$2.3M
Agilent Technologies (Agilent) 4814HHS | NIH | National Cancer Institute (NCI) T32CA009056HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI) P01HL146358HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI) R01HL157710HHS | NIH | National Institute of Allergy and Infectious Diseases (NIAID) R01AI173214HHS | NIH | National Institute of General Medical Sciences (NIGMS) R35GM138003HHS | NIH | National Institute of General Medical Sciences (NIGMS) T32GM136614NCI NIH HHS T32 CA009056NIGMS NIH HHS R35 GM138003NIGMS NIH HHS T32 GM136614W. M. Keck Foundation (WMKF) 995337
6 · The paper itself

Abstract

Metabolites and metabolic cofactors can shape the innate immune response, though the pathways by which these molecules adjust inflammation remain incompletely understood. Here we show that the metabolic cofactor coenzyme A (CoA) enhances IL-4 driven alternative macrophage activation [M(IL-4)] in vitro and in vivo. Unexpectedly, we find that perturbations in intracellular CoA metabolism do not influence M(IL-4) differentiation. Rather, we discover that exogenous CoA is a weak TLR4 agonist which primes macrophages for increased receptivity to IL-4 signals and resolution of inflammation via MyD88. Mechanistic studies reveal MyD88-linked signals enhance IL-4 responsiveness, in part, by reshaping chromatin accessibility to enhance transcription of IL-4-linked genes. The results identify CoA as a host metabolic co-factor that influences macrophage function through an extrinsic TLR4-dependent mechanism and suggest that damage-associated molecular patterns (DAMPs) can prime macrophages for alternative activation and resolution of inflammation.

Identifiers

PMID42760443

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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.