c-Kit signaling potentiates CAR T cell efficacy in solid tumors by CD28- and IL-2-independent co-stimulation.


Journal

Nature cancer
ISSN: 2662-1347
Titre abrégé: Nat Cancer
Pays: England
ID NLM: 101761119

Informations de publication

Date de publication:
07 2023
Historique:
received: 30 06 2022
accepted: 08 05 2023
medline: 27 7 2023
pubmed: 20 6 2023
entrez: 19 6 2023
Statut: ppublish

Résumé

The limited efficacy of chimeric antigen receptor (CAR) T cell therapy for solid tumors necessitates engineering strategies that promote functional persistence in an immunosuppressive environment. Herein, we use c-Kit signaling, a physiological pathway associated with stemness in hematopoietic progenitor cells (T cells lose expression of c-Kit during differentiation). CAR T cells with intracellular expression, but no cell-surface receptor expression, of the c-Kit D816V mutation (KITv) have upregulated STAT phosphorylation, antigen activation-dependent proliferation and CD28- and interleukin-2-independent and interferon-γ-mediated co-stimulation, augmenting the cytotoxicity of first-generation CAR T cells. This translates to enhanced survival, including in transforming growth factor-β-rich and low-antigen-expressing solid tumor models. KITv CAR T cells have equivalent or better in vivo efficacy than second-generation CAR T cells and are susceptible to tyrosine kinase inhibitors (safety switch). When combined with CD28 co-stimulation, KITv co-stimulation functions as a third signal, enhancing efficacy and providing a potent approach to treat solid tumors.

Identifiants

pubmed: 37336986
doi: 10.1038/s43018-023-00573-4
pii: 10.1038/s43018-023-00573-4
doi:

Substances chimiques

CD28 Antigens 0
Interleukin-2 0
Receptor Protein-Tyrosine Kinases EC 2.7.10.1
Proto-Oncogene Proteins c-kit EC 2.7.10.1

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, Non-P.H.S.

Langues

eng

Sous-ensembles de citation

IM

Pagination

1001-1015

Subventions

Organisme : NCI NIH HHS
ID : P30 CA008748
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA235667
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA236615
Pays : United States
Organisme : NCI NIH HHS
ID : U01 CA214195
Pays : United States

Informations de copyright

© 2023. The Author(s), under exclusive licence to Springer Nature America, Inc.

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Auteurs

Yuquan Xiong (Y)

Thoracic Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, NY, USA.

Meriem Taleb (M)

Thoracic Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, NY, USA.

Kyohei Misawa (K)

Thoracic Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, NY, USA.

Zhaohua Hou (Z)

Thoracic Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, NY, USA.

Srijita Banerjee (S)

Thoracic Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, NY, USA.

Alfredo Amador-Molina (A)

Thoracic Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, NY, USA.

David R Jones (DR)

Thoracic Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, NY, USA.

Navin K Chintala (NK)

Thoracic Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, NY, USA.

Prasad S Adusumilli (PS)

Thoracic Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, NY, USA. adusumip@mskcc.org.
Center for Cell Engineering, Memorial Sloan Kettering Cancer Center, New York, NY, USA. adusumip@mskcc.org.

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