Evidence map›Paper›PMID 38438357›Full record

ArticleNature communications2024

Inactivation of cytidine triphosphate synthase 1 prevents fatal auto-immunity in mice.

Claire Soudais, Romane Schaus, Camille Bachelet, Norbert Minet, Sara Mouasni, Cécile Garcin, Caique Lopes Souza, Pierre David, Clara Cousu, Hélène Asnagli and 8 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

5 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Age-Associated Metabolomic Changes in Human Spermatozoa.International journal of molecular sciences · 2026
    Article
  3. Article
  4. Cytoophidium complexes resonate with cell fates.Cellular and molecular life sciences : CMLS · 2025
    Article
  5. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

18 authors at 2 institutions in 1 country.

Claire SoudaisLaboratory of Lymphocyte Activation and Susceptibility to EBV infection, Inserm UMR 1163, Institut Imagine, Paris, France. claire.soudais@inserm.fr.ORCID 0000-0002-4387-6649
Romane SchausLaboratory of Lymphocyte Activation and Susceptibility to EBV infection, Inserm UMR 1163, Institut Imagine, Paris, France.
Camille BacheletLaboratory of Lymphocyte Activation and Susceptibility to EBV infection, Inserm UMR 1163, Institut Imagine, Paris, France.ORCID 0000-0003-3800-3816
Norbert MinetLaboratory of Lymphocyte Activation and Susceptibility to EBV infection, Inserm UMR 1163, Institut Imagine, Paris, France.ORCID 0000-0003-3570-4166
Sara MouasniLaboratory of Molecular Basis of Altered Immune Homeostasis Inserm UMR 1163, Institut Imagine, Paris, France.
Cécile GarcinLaboratory of Lymphocyte Activation and Susceptibility to EBV infection, Inserm UMR 1163, Institut Imagine, Paris, France.
Caique Lopes SouzaLaboratory of Lymphocyte Activation and Susceptibility to EBV infection, Inserm UMR 1163, Institut Imagine, Paris, France.
Pierre DavidTransgenesis Platform, Laboratoire d'Expérimentation Animale et Transgenèse (LEAT), Institut Imagine-Structure Fédérative de Recherche Necker INSERM US24/CNRS, UMS3633, Paris, France.ORCID 0009-0006-1611-5648
Clara CousuUniversité Paris Cité, CNRS UMR 8253, INSERM U1151, Institut Necker Enfants Malades, F-75015, Paris, France.
Hélène AsnagliStep-Pharma, Technoparc du Pays-de-Gex, Saint-Genis-Pouilly, France.
Andrew ParkerStep-Pharma, Technoparc du Pays-de-Gex, Saint-Genis-Pouilly, France.
Paul Palmquist-GomesUniversité de Paris Cité, Paris, France.
Fernando E SepulvedaLaboratory of Molecular Basis of Altered Immune Homeostasis Inserm UMR 1163, Institut Imagine, Paris, France.ORCID 0000-0001-5865-4929
Sébastien StorckUniversité Paris Cité, CNRS UMR 8253, INSERM U1151, Institut Necker Enfants Malades, F-75015, Paris, France.ORCID 0000-0002-2682-5962
Sigolène M MeilhacUniversité de Paris Cité, Paris, France.
Alain Fischer *Laboratory of Lymphocyte Activation and Susceptibility to EBV infection, Inserm UMR 1163, Institut Imagine, Paris, France.
Emmanuel Martin *Laboratory of Lymphocyte Activation and Susceptibility to EBV infection, Inserm UMR 1163, Institut Imagine, Paris, France.ORCID 0000-0003-4211-7373
Sylvain LatourLaboratory of Lymphocyte Activation and Susceptibility to EBV infection, Inserm UMR 1163, Institut Imagine, Paris, France. sylvain.latour@inserm.fr.ORCID 0000-0001-8238-4391
Inserm · FRCentre National de la Recherche Scientifique · FR

Funding

Agence Nationale de la Recherche (French National Research Agency) ANR-21-CE15-0018-01EC | EU Framework Programme for Research and Innovation H2020 | H2020 Priority Excellent Science | H2020 European Research Council (H2020 Excellent Science - European Research Council) ERC-2015-PoC_680465_SAFEIMMUNOSUPPRESSEC | EU Framework Programme for Research and Innovation H2020 | H2020 Priority Excellent Science | H2020 European Research Council (H2020 Excellent Science - European Research Council) ERC-2015-PoC_MasterLigue Contre le Cancer Equipe labelisée
6 · The paper itself

Abstract

De novo synthesis of the pyrimidine, cytidine triphosphate (CTP), is crucial for DNA/RNA metabolism and depends on the CTP synthetases, CTPS1 and -2. Partial CTPS1 deficiency in humans has previously been shown to lead to immunodeficiency, with impaired expansion of T and B cells. Here, we examine the effects of conditional and inducible inactivation of Ctps1 and/or Ctps2 on mouse embryonic development and immunity. We report that deletion of Ctps1, but not Ctps2, is embryonic-lethal. Tissue and cells with high proliferation and renewal rates, such as intestinal epithelium, erythroid and thymic lineages, activated B and T lymphocytes, and memory T cells strongly rely on CTPS1 for their maintenance and growth. However, both CTPS1 and CTPS2 are required for T cell proliferation following TCR stimulation. Deletion of Ctps1 in T cells or treatment with a CTPS1 inhibitor rescued Foxp3-deficient mice from fatal systemic autoimmunity and reduced the severity of experimental autoimmune encephalomyelitis. These findings support that CTPS1 may represent a target for immune suppression.

Indexed as

AutoimmunityEmbryonic DevelopmentAnimalsB-LymphocytesCell ProliferationCytidine TriphosphateFemaleHumansMicePregnancyCytidine Triphosphate

Identifiers

PMID38438357
PMCPMC10912214
OpenAlexW4392367661

What OpenQuestion holds

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LicenceCC BY
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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.