Tumor reactive γδ T cells contribute to a complete response to PD-1 blockade in a Merkel cell carcinoma patient

Scott C. Lien, Dalam Ly, S. Y. Cindy Yang, Ben X. Wang, Derek L. Clouthier, Michael St. Paul, Ramy Gadalla, Babak Noamani, Carlos R. Garcia-Batres, Sarah Boross-Harmer, Philippe L. Bedard, Trevor J. Pugh, Anna Spreafico, Naoto Hirano, Albiruni R. A. Razak and Pamela S. Ohashi ()
Additional contact information
Scott C. Lien: University Health Network
Dalam Ly: University Health Network
S. Y. Cindy Yang: University Health Network
Ben X. Wang: University Health Network
Derek L. Clouthier: University Health Network
Michael St. Paul: University Health Network
Ramy Gadalla: University Health Network
Babak Noamani: University Health Network
Carlos R. Garcia-Batres: University Health Network
Sarah Boross-Harmer: University of Toronto
Philippe L. Bedard: University of Toronto
Trevor J. Pugh: University Health Network
Anna Spreafico: University of Toronto
Naoto Hirano: University Health Network
Albiruni R. A. Razak: University of Toronto
Pamela S. Ohashi: University Health Network

Nature Communications, 2024, vol. 15, issue 1, 1-11

Abstract: Abstract Immunotherapies targeting PD-1/PD-L1 are now widely used in the clinic to treat a variety of malignancies. While most of the research on T cell exhaustion and PD-1 blockade has been focused on conventional αβ T cells, the contribution of innate-like T cells such as γδ T cells to anti-PD-1/PD-L1 mediated therapy is limited. Here we show that tumor reactive γδ T cells respond to PD-1 blockade in a Merkel cell carcinoma (MCC) patient experiencing a complete response to therapy. We find clonally expanded γδ T cells in the blood and tumor after pembrolizumab treatment, and this Vγ2Vδ1 clonotype recognizes Merkel cancer cells in a TCR-dependent manner. Notably, the intra-tumoral γδ T cells in the MCC patient are characterized by higher expression of PD-1 and TIGIT, relative to conventional CD4 and CD8 T cells. Our results demonstrate that innate-like T cells could also contribute to an anti-tumor response after PD-1 blockade.

Date: 2024
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DOI: 10.1038/s41467-024-45449-y

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