Figure S5 from Vγ9Vδ2 T Cells Express an Antitumor Profile Associated with Anti–PD-(L)1 Responses and Activation Defects Restored by Anti-BTN3A in Triple-Negative Breast Cancer

Q: What type of study is this?

This is a Quantitative Study study.

Stéphane Fattori; Laurent Gorvel; Marie-Sarah Rouviére; Samuel Granjeaud; Amira Ben Amara; Manon Richaud; Nicolas Boucherit; Carole Tarpin; Jihane Pakradouni; Julien Hédou; Grégoire Bellan; Brice Gaudillière; Emmanuelle Charafe‐Jauffret; Gilles Houvenaeghel; Éric Lambaudie; François Bertucci; Jean‐Jacques Fournié; Anthony Gonçalvès; Philippe Rochigneux; Anne-Sophie Chrétien; Daniel Olive

doi:10.1158/2326-6066.30255247

Key Points

vg9vd2 t cells demonstrate a strong antitumor profile in triple-negative breast cancer, suggesting new therapeutic avenues.
Transcriptional profiling indicates vg9vd2 t cells possess type-I cytotoxic activity in untreated cases of triple-negative breast cancer.
The administration of anti-btn3a restores activation defects in vg9vd2 t cells, potentially enhancing their therapeutic effectiveness.
Findings imply that modulating vg9vd2 t cell activity may significantly improve anti–pd-l1 treatment outcomes in triple-negative breast cancer.

Implication

Observational analysis shows vg9vd2 t cells enhance antitumor activity in triple-negative breast cancer, highlighting the potential of anti–pd-l1 and btn3a therapies.

Abstract

Vg9Vd2 T cells are transcriptionally armed for type–I antitumor cytotoxic activity in untreated TNBC (related to Figure 2)

Discussion

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Cite This Study

Fattori et al. (2025) studied this question.

synapsesocial.com/papers/68e040f7a99c246f578b3d60 https://doi.org/10.1158/2326-6066.30255247

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Figure S5 from Vγ9Vδ2 T Cells Express an Antitumor Profile Associated with Anti–PD-(L)1 Responses and Activation Defects Restored by Anti-BTN3A in Triple-Negative Breast Cancer

Key Points

Implication

Abstract

Discussion

Cite This Study

Figure S5 from Vγ9Vδ2 T Cells Express an Antitumor Profile Associated with Anti–PD-(L)1 Responses and Activation Defects Restored by Anti-BTN3A in Triple-Negative Breast Cancer

Key Points

Implication

Abstract

Discussion

Cite This Study

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