Evidence map›Paper›PMID 42362565›Full record

ArticleNature communications2026

Multiomic analysis identifies glutaminolysis-dependent metabolic enhancement of immune memory utilised for vaccine development.

J M Sowerby, P Kotagiri, S Clare, D Griffiths, O Knight, I Cuthbertson, K Harcourt, P Pereyra Gerber, I Pshenichnaya, C Connor and 15 more

Abstract read
In one paragraph

Article in Nature communications, 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

25 authors.

J M Sowerby *Cambridge Institute of Therapeutic Immunology and Infectious Disease, Jeffrey Cheah Biomedical Centre, Cambridge, UK.
P Kotagiri *Cambridge Institute of Therapeutic Immunology and Infectious Disease, Jeffrey Cheah Biomedical Centre, Cambridge, UK.ORCID http://orcid.org/0000-0002-9806-4349
S ClareCambridge Institute of Therapeutic Immunology and Infectious Disease, Jeffrey Cheah Biomedical Centre, Cambridge, UK.
D GriffithsCambridge Institute of Therapeutic Immunology and Infectious Disease, Jeffrey Cheah Biomedical Centre, Cambridge, UK.ORCID http://orcid.org/0009-0001-5312-511X
O KnightCambridge Institute of Therapeutic Immunology and Infectious Disease, Jeffrey Cheah Biomedical Centre, Cambridge, UK.ORCID http://orcid.org/0000-0002-0424-2379
I CuthbertsonCambridge Institute of Therapeutic Immunology and Infectious Disease, Jeffrey Cheah Biomedical Centre, Cambridge, UK.ORCID http://orcid.org/0000-0002-0245-4466
K HarcourtWellcome Sanger Institute, Wellcome Genome Campus, Hinxton, Cambridge, UK.
P Pereyra GerberCambridge Institute of Therapeutic Immunology and Infectious Disease, Jeffrey Cheah Biomedical Centre, Cambridge, UK.
I PshenichnayaCambridge Institute of Therapeutic Immunology and Infectious Disease, Jeffrey Cheah Biomedical Centre, Cambridge, UK.
C ConnorCambridge Institute of Therapeutic Immunology and Infectious Disease, Jeffrey Cheah Biomedical Centre, Cambridge, UK.
A DentonCambridge Institute of Therapeutic Immunology and Infectious Disease, Jeffrey Cheah Biomedical Centre, Cambridge, UK.ORCID http://orcid.org/0000-0002-4580-3443
G A StollCambridge Institute of Therapeutic Immunology and Infectious Disease, Jeffrey Cheah Biomedical Centre, Cambridge, UK.ORCID http://orcid.org/0000-0003-2531-9168
C MataraDepartment of Medicine, University of Cambridge School of Clinical Medicine, Cambridge, UK.
C KeelNational Institute for Health Research Cambridge Centre for Clinical Research, Cambridge, UK.
G ManferrariCambridge Institute of Therapeutic Immunology and Infectious Disease, Jeffrey Cheah Biomedical Centre, Cambridge, UK.
T BirkleCambridge Institute of Therapeutic Immunology and Infectious Disease, Jeffrey Cheah Biomedical Centre, Cambridge, UK.
P NaydenovaCambridge Institute of Therapeutic Immunology and Infectious Disease, Jeffrey Cheah Biomedical Centre, Cambridge, UK.
H PeckWHO Collaborating Centre for Reference and Research on Influenza (VIDRL), Peter Doherty Institute for Infection and Immunity, 792 Elizabeth Street, Melbourne, Australia.
P A LyonsCambridge Institute of Therapeutic Immunology and Infectious Disease, Jeffrey Cheah Biomedical Centre, Cambridge, UK.ORCID http://orcid.org/0000-0001-7035-8997
I BarrWHO Collaborating Centre for Reference and Research on Influenza (VIDRL), Peter Doherty Institute for Infection and Immunity, 792 Elizabeth Street, Melbourne, Australia.ORCID http://orcid.org/0000-0002-7351-418X
Y ModisCambridge Institute of Therapeutic Immunology and Infectious Disease, Jeffrey Cheah Biomedical Centre, Cambridge, UK.ORCID http://orcid.org/0000-0002-6084-0429
G DouganCambridge Institute of Therapeutic Immunology and Infectious Disease, Jeffrey Cheah Biomedical Centre, Cambridge, UK.
N J MathesonCambridge Institute of Therapeutic Immunology and Infectious Disease, Jeffrey Cheah Biomedical Centre, Cambridge, UK.ORCID http://orcid.org/0000-0002-3318-1851
K G C SmithCambridge Institute of Therapeutic Immunology and Infectious Disease, Jeffrey Cheah Biomedical Centre, Cambridge, UK.ORCID http://orcid.org/0000-0003-3829-4326
E F McKinneyCambridge Institute of Therapeutic Immunology and Infectious Disease, Jeffrey Cheah Biomedical Centre, Cambridge, UK. efm30@cam.ac.uk.ORCID http://orcid.org/0000-0003-3516-3072

Funding

CUH | Addenbrooke's Charitable Trust, Cambridge University Hospitals (Addenbrooke's Charitable Trust, Cambridge University Hospitals NHS Foundation Trust) 900299DH | National Institute for Health Research (NIHR) RC 1110564Wellcome TrustWellcome Trust (Wellcome) 10406/Z/14/Z
6 · The paper itself

Abstract

Vaccines work by inducing an immunological memory response to protect against infection or disease. More effective vaccines are required to improve protection of high-risk groups such as the elderly. Here we screen transcriptional signatures of T cell memory against repurposable drug signatures, identifying a subclass of lysine deacetylase inhibitors (KDACi) capable of promoting a memory precursor phenotype in primary T cells. Leveraging combined acetylomic, metabolomic, transcriptomic and epigenomic analyses, we identify enhanced glutaminolysis as the mechanism responsible for the KDACi effect, with selective inhibition reversing the changes induced by KDACi treatment. We validate the ability of a repurposable KDACi (sodium valproate) to promote immune memory in four murine models of infection and immunisation, with the effect reversed by concurrently inhibiting glutaminolysis. Finally, we undertake a human challenge study, which demonstrates a 10-fold increase in correlates of protection following seasonal influenza vaccination. These results reveal immune-metabolic adjuvant properties of repurposable lysine deacetylase inhibitors and demonstrate that systematic screening can identify both efficacy and mechanism of repurposable drugs.

Indexed as

GlutamineImmunologic MemoryInfluenza VaccinesAnimalsFemaleHistone Deacetylase InhibitorsHumansMetabolomicsMiceMice, Inbred C57BLMultiomicsT-LymphocytesValproic AcidGlutamineHistone Deacetylase InhibitorsInfluenza VaccinesValproic Acid

Identifiers

PMID42362565
PMCPMC13454449

What OpenQuestion holds

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Registered trials

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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.