Self-activation of Vγ9Vδ2 T cells by exogenous phosphoantigens involves TCR and butyrophilins.


Journal

Cellular & molecular immunology
ISSN: 2042-0226
Titre abrégé: Cell Mol Immunol
Pays: China
ID NLM: 101242872

Informations de publication

Date de publication:
08 2021
Historique:
received: 30 03 2021
accepted: 04 06 2021
pubmed: 30 6 2021
medline: 1 4 2022
entrez: 29 6 2021
Statut: ppublish

Résumé

The high cytotoxic activity of Vγ9Vδ2 T lymphocytes against tumor cells makes them useful candidates in anticancer therapies. However, the molecular mechanism of their activation by phosphoantigens (PAgs) is not completely known. Many studies have depicted the mechanism of Vγ9Vδ2 T-cell activation by PAg-sensed accessory cells, such as immune presenting cells or tumor cells. In this study, we demonstrated that pure resting Vγ9Vδ2 T lymphocytes can self-activate through exogenous PAgs, involving their TCR and the butyrophilins BTN3A1 and BTN2A1. This is the first time that these three molecules, concurrently expressed at the plasma membrane of Vγ9Vδ2 T cells, have been shown to be involved together on the same and unique T cell during PAg activation. Moreover, the use of probucol to stimulate the inhibition of this self-activation prompted us to propose that ABCA-1 could be implicated in the transfer of exogenous PAgs inside Vγ9Vδ2 T cells before activating them through membrane clusters formed by γ9TCR, BTN3A1 and BTN2A1. The self-activation of Vγ9Vδ2 T cells, which leads to self-killing, can therefore participate in the failure of γδ T cell-based therapies with exogenous PAgs and should be taken into account.

Identifiants

pubmed: 34183807
doi: 10.1038/s41423-021-00720-w
pii: 10.1038/s41423-021-00720-w
pmc: PMC8237548
doi:

Substances chimiques

Antigens, CD 0
Butyrophilins 0
Receptors, Antigen, T-Cell, gamma-delta 0

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

1861-1870

Informations de copyright

© 2021. The Author(s), under exclusive licence to CSI and USTC.

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Auteurs

Chloé Laplagne (C)

Inserm UMR1037, Centre de Recherches en Cancérologie de Toulouse, Toulouse, France.
Université Toulouse III Paul-Sabatier, Toulouse, France.
ERL 5294 CNRS, Toulouse, France.

Laetitia Ligat (L)

Inserm UMR1037, Centre de Recherches en Cancérologie de Toulouse, Toulouse, France.
Université Toulouse III Paul-Sabatier, Toulouse, France.
ERL 5294 CNRS, Toulouse, France.

Juliet Foote (J)

Inserm UMR1037, Centre de Recherches en Cancérologie de Toulouse, Toulouse, France.
Université Toulouse III Paul-Sabatier, Toulouse, France.
ERL 5294 CNRS, Toulouse, France.

Frederic Lopez (F)

Inserm UMR1037, Centre de Recherches en Cancérologie de Toulouse, Toulouse, France.
Université Toulouse III Paul-Sabatier, Toulouse, France.
ERL 5294 CNRS, Toulouse, France.

Jean-Jacques Fournié (JJ)

Inserm UMR1037, Centre de Recherches en Cancérologie de Toulouse, Toulouse, France.
Université Toulouse III Paul-Sabatier, Toulouse, France.
ERL 5294 CNRS, Toulouse, France.

Camille Laurent (C)

Inserm UMR1037, Centre de Recherches en Cancérologie de Toulouse, Toulouse, France.
Université Toulouse III Paul-Sabatier, Toulouse, France.
ERL 5294 CNRS, Toulouse, France.
IUCT-O, Toulouse, France.

Salvatore Valitutti (S)

Inserm UMR1037, Centre de Recherches en Cancérologie de Toulouse, Toulouse, France.
Université Toulouse III Paul-Sabatier, Toulouse, France.
ERL 5294 CNRS, Toulouse, France.

Mary Poupot (M)

Inserm UMR1037, Centre de Recherches en Cancérologie de Toulouse, Toulouse, France. mary.poupot@inserm.fr.
Université Toulouse III Paul-Sabatier, Toulouse, France. mary.poupot@inserm.fr.
ERL 5294 CNRS, Toulouse, France. mary.poupot@inserm.fr.

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