Evidence map›Paper›PMID 38702311›Full record

ArticleNature communications2024

CD74 supports accumulation and function of regulatory T cells in tumors.

Elisa Bonnin, Maria Rodrigo Riestra, Federico Marziali, Rafael Mena Osuna, Jordan Denizeau, Mathieu Maurin, Juan Jose Saez, Mabel Jouve, Pierre-Emmanuel Bonté, Wilfrid Richer and 13 more

Abstract 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. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing 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

46 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Targeted Inhibition of CD74Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. 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

23 authors.

Elisa BonninINSERM U932 Immunity and Cancer, PSL University, Institut Curie Research Center, Paris, France.ORCID http://orcid.org/0009-0005-6544-2736
Maria Rodrigo RiestraINSERM U932 Immunity and Cancer, PSL University, Institut Curie Research Center, Paris, France.
Federico MarzialiINSERM U932 Immunity and Cancer, PSL University, Institut Curie Research Center, Paris, France.
Rafael Mena OsunaINSERM U932 Immunity and Cancer, PSL University, Institut Curie Research Center, Paris, France.
Jordan DenizeauINSERM U932 Immunity and Cancer, PSL University, Institut Curie Research Center, Paris, France.
Mathieu MaurinINSERM U932 Immunity and Cancer, PSL University, Institut Curie Research Center, Paris, France.
Juan Jose SaezINSERM U932 Immunity and Cancer, PSL University, Institut Curie Research Center, Paris, France.ORCID http://orcid.org/0000-0001-6708-6724
Mabel JouveINSERM U932 Immunity and Cancer, PSL University, Institut Curie Research Center, Paris, France.
Pierre-Emmanuel BontéINSERM U932 Immunity and Cancer, PSL University, Institut Curie Research Center, Paris, France.ORCID http://orcid.org/0000-0002-9732-5826
Wilfrid RicherINSERM U932 Immunity and Cancer, PSL University, Institut Curie Research Center, Paris, France.
Fabien NevoEgle Therapeutics, Paris, France.
Sebastien LemoineEgle Therapeutics, Paris, France.
Nicolas GirardINSERM U932 Immunity and Cancer, PSL University, Institut Curie Research Center, Paris, France.
Marine LefevrePathology Department, Institut Mutualiste Montsouris, Paris, France.
Edith BorcomanDepartment of Drug Development and Innovation (D3i), Institut Curie, Paris, France.
Anne Vincent-SalomonInstitut du Thorax Curie Montsouris, Institut Curie, Paris, France.ORCID http://orcid.org/0000-0001-5754-5771
Sylvain BaulandeInstitut Curie Genomics of Excellence (ICGex) Platform, PSL Research University, Institut Curie Research Center, Paris, France.ORCID http://orcid.org/0000-0003-3104-1684
Helene D MoreauINSERM U932 Immunity and Cancer, PSL University, Institut Curie Research Center, Paris, France.
Christine SedlikINSERM U932 Immunity and Cancer, PSL University, Institut Curie Research Center, Paris, France.
Claire HivrozINSERM U932 Immunity and Cancer, PSL University, Institut Curie Research Center, Paris, France.ORCID http://orcid.org/0000-0002-6794-2890
Ana-Maria Lennon-DuménilINSERM U932 Immunity and Cancer, PSL University, Institut Curie Research Center, Paris, France.
Jimena Tosello BoariINSERM U932 Immunity and Cancer, PSL University, Institut Curie Research Center, Paris, France. jimena.tosello@curie.fr.ORCID http://orcid.org/0000-0003-1563-4420
Eliane PiaggioINSERM U932 Immunity and Cancer, PSL University, Institut Curie Research Center, Paris, France. eliane.piaggio@curie.fr.ORCID http://orcid.org/0000-0002-2455-8442

Funding

Agence Nationale de la Recherche (French National Research Agency) ANR-10-IDEX-0001-02 PSLAgence Nationale de la Recherche (French National Research Agency) ANR-11-LABX-0043
6 · The paper itself

Abstract

Regulatory T cells (Tregs) are plastic cells playing a pivotal role in the maintenance of immune homeostasis. Tregs actively adapt to the microenvironment where they reside; as a consequence, their molecular and functional profiles differ among tissues and pathologies. In tumors, the features acquired by Tregs remains poorly characterized. Here, we observe that human tumor-infiltrating Tregs selectively overexpress CD74, the MHC class II invariant chain. CD74 has been previously described as a regulator of antigen-presenting cell biology, however its function in Tregs remains unknown. CD74 genetic deletion in human primary Tregs reveals that CD74KO Tregs exhibit major defects in the organization of their actin cytoskeleton and intracellular organelles. Additionally, intratumoral CD74KO Tregs show a decreased activation, a drop in Foxp3 expression, a low accumulation in the tumor, and consistently, they are associated with accelerated tumor rejection in preclinical models in female mice. These observations are unique to tumor conditions as, at steady state, CD74KO-Treg phenotype, survival, and suppressive capacity are unaffected in vitro and in vivo. CD74 therefore emerges as a specific regulator of tumor-infiltrating Tregs and as a target to interfere with Treg anti-tumor activity.

Indexed as

Antigens, Differentiation, B-LymphocyteHistocompatibility Antigens Class IIT-Lymphocytes, RegulatoryAnimalsFemaleForkhead Transcription FactorsHumansLymphocytes, Tumor-InfiltratingMiceMice, Inbred C57BLMice, KnockoutNeoplasmsTumor MicroenvironmentAntigens, Differentiation, B-LymphocyteForkhead Transcription FactorsFOXP3 protein, humanHistocompatibility Antigens Class IIinvariant chain

Identifiers

PMID38702311
PMCPMC11068745

What OpenQuestion holds

Textmetadata
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.