Complementarity-determining region clustering may cause CAR-T cell dysfunction.


Journal

Nature communications
ISSN: 2041-1723
Titre abrégé: Nat Commun
Pays: England
ID NLM: 101528555

Informations de publication

Date de publication:
10 08 2023
Historique:
received: 20 12 2021
accepted: 19 07 2023
medline: 14 8 2023
pubmed: 11 8 2023
entrez: 10 8 2023
Statut: epublish

Résumé

Chimeric antigen receptor (CAR)-T cell therapy is rapidly advancing as cancer treatment, however, designing an optimal CAR remains challenging. A single-chain variable fragment (scFv) is generally used as CAR targeting moiety, wherein the complementarity-determining regions (CDRs) define its specificity. We report here that the CDR loops can cause CAR clustering, leading to antigen-independent tonic signalling and subsequent CAR-T cell dysfunction. We show via CARs incorporating scFvs with identical framework and varying CDR sequences that CARs may cluster on the T cell surface, which leads to antigen-independent CAR-T cell activation, characterized by increased cell size and interferon (IFN)-γ secretion. This results in CAR-T cell exhaustion, activation-induced cell death and reduced responsiveness to target-antigen-expressing tumour cells. CDR mutagenesis confirms that the CAR-clustering is mediated by CDR-loops. In summary, antigen-independent tonic signalling can be induced by CDR-mediated CAR clustering, which could not be predicted from the scFv sequences, but could be tested for by evaluating the activity of unstimulated CAR-T cells.

Identifiants

pubmed: 37563127
doi: 10.1038/s41467-023-40303-z
pii: 10.1038/s41467-023-40303-z
pmc: PMC10415375
doi:

Substances chimiques

Complementarity Determining Regions 0
Single-Chain Antibodies 0
Receptors, Antigen, T-Cell 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

4732

Informations de copyright

© 2023. Springer Nature Limited.

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Auteurs

Tina Sarén (T)

Uppsala University, Dept Immunology, Genetics, Pathology, Science for Life Laboratory, Uppsala, Sweden.

Giulia Saronio (G)

Uppsala University, Dept Immunology, Genetics, Pathology, Science for Life Laboratory, Uppsala, Sweden.

Paula Marti Torrell (P)

Uppsala University, Dept Immunology, Genetics, Pathology, Science for Life Laboratory, Uppsala, Sweden.

Xu Zhu (X)

Uppsala University, Dept Immunology, Genetics, Pathology, Science for Life Laboratory, Uppsala, Sweden.

Josefin Thelander (J)

Uppsala University, Dept Immunology, Genetics, Pathology, Science for Life Laboratory, Uppsala, Sweden.

Yasmin Andersson (Y)

Royal Institute of Technology (KTH), Drug Discovery and Development Platform, Science for Life Laboratory, Solna, Sweden.

Camilla Hofström (C)

Royal Institute of Technology (KTH), Drug Discovery and Development Platform, Science for Life Laboratory, Solna, Sweden.

Marika Nestor (M)

Uppsala University, Dept Immunology, Genetics, Pathology, Science for Life Laboratory, Uppsala, Sweden.

Anna Dimberg (A)

Uppsala University, Dept Immunology, Genetics, Pathology, Science for Life Laboratory, Uppsala, Sweden.

Helena Persson (H)

Royal Institute of Technology (KTH), Drug Discovery and Development Platform, Science for Life Laboratory, Solna, Sweden.

Mohanraj Ramachandran (M)

Uppsala University, Dept Immunology, Genetics, Pathology, Science for Life Laboratory, Uppsala, Sweden.

Di Yu (D)

Uppsala University, Dept Immunology, Genetics, Pathology, Science for Life Laboratory, Uppsala, Sweden. di.yu@igp.uu.se.

Magnus Essand (M)

Uppsala University, Dept Immunology, Genetics, Pathology, Science for Life Laboratory, Uppsala, Sweden. magnus.essand@igp.uu.se.

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