IFNγ Helps CBLB-Deficient CD8+ T Cells to Put Up Resistance to Tregs.


Journal

Cancer immunology research
ISSN: 2326-6074
Titre abrégé: Cancer Immunol Res
Pays: United States
ID NLM: 101614637

Informations de publication

Date de publication:
01 04 2022
Historique:
entrez: 1 4 2022
pubmed: 2 4 2022
medline: 5 4 2022
Statut: ppublish

Résumé

In this issue, Han and colleagues demonstrate in preclinical cancer models that genetic deletion of the E3 ubiquitin ligase Cbl proto-oncogene B (CBLB) in adoptively transferred CD8+ T cells induces resistance to regulatory T cells. CBLB deletion induces IFNγ and downmodulates TGFβ/SMAD signaling. This ultimately enforces these cells to be way more effective against various cancers. See related article by Han et al., p. 437 (4).

Identifiants

pubmed: 35362047
pii: 689537
doi: 10.1158/2326-6066.CIR-22-0080
doi:

Substances chimiques

Adaptor Proteins, Signal Transducing 0
Interferon-gamma 82115-62-6
Proto-Oncogene Proteins c-cbl EC 2.3.2.27
Ubiquitin-Protein Ligases EC 2.3.2.27

Banques de données

ClinicalTrials.gov
['NCT05107674', 'NCT03087591']

Types de publication

Editorial Comment

Langues

eng

Sous-ensembles de citation

IM

Pagination

370

Commentaires et corrections

Type : CommentOn

Informations de copyright

©2022 American Association for Cancer Research.

Auteurs

Dominik Wolf (D)

Department of Internal Medicine V, Hematology and Oncology, Comprehensive Cancer Center Innsbruck (CCCI) and Tyrolean Cancer Research Institute (TKFI), Medical University of Innsbruck, Innsbruck, Austria.

Gottfried Baier (G)

Institute of Cell Genetics, Department for Genetics, Medical University of Innsbruck, Innsbruck, Austria.

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Classifications MeSH