Tumour and host cell PD-L1 is required to mediate suppression of anti-tumour immunity in mice

Janet Lau, Jeanne Cheung, Armando Navarro, Steve Lianoglou, Benjamin Haley, Klara Totpal, Laura Sanders, Hartmut Koeppen, Patrick Caplazi, Jacqueline McBride, Henry Chiu, Rebecca Hong, Jane Grogan, Vincent Javinal, Robert Yauch, Bryan Irving, Marcia Belvin, Ira Mellman, Jeong M. Kim () and Maike Schmidt ()
Additional contact information
Janet Lau: Genentech, Inc.
Jeanne Cheung: Genentech, Inc.
Armando Navarro: Genentech, Inc.
Steve Lianoglou: Genentech, Inc.
Benjamin Haley: Genentech, Inc.
Klara Totpal: Genentech, Inc.
Laura Sanders: Genentech, Inc.
Hartmut Koeppen: Genentech, Inc.
Patrick Caplazi: Genentech, Inc.
Jacqueline McBride: Genentech, Inc.
Henry Chiu: Genentech, Inc.
Rebecca Hong: Genentech, Inc.
Jane Grogan: Genentech, Inc.
Vincent Javinal: Genentech, Inc.
Robert Yauch: Genentech, Inc. 1 DNA Way
Bryan Irving: Genentech, Inc.
Marcia Belvin: Genentech, Inc.
Ira Mellman: Genentech, Inc.
Jeong M. Kim: Genentech, Inc.
Maike Schmidt: Genentech, Inc.

Nature Communications, 2017, vol. 8, issue 1, 1-11

Abstract: Abstract Expression of PD-L1, the ligand for T-cell inhibitory receptor PD-1, is one key immunosuppressive mechanism by which cancer avoids eradication by the immune system. Therapeutic use of blocking antibodies to PD-L1 or its receptor PD-1 has produced unparalleled, durable clinical responses, with highest likelihood of response seen in patients whose tumour or immune cells express PD-L1 before therapy. The significance of PD-L1 expression in each cell type has emerged as a central and controversial unknown in the clinical development of immunotherapeutics. Using genetic deletion in preclinical mouse models, here we show that PD-L1 from disparate cellular sources, including tumour cells, myeloid or other immune cells can similarly modulate the degree of cytotoxic T-cell function and activity in the tumour microenvironment. PD-L1 expression in both the host and tumour compartment contribute to immune suppression in a non-redundant fashion, suggesting that both sources could be predictive of sensitivity to therapeutic agents targeting the PD-L1/PD-1 axis.

Date: 2017
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DOI: 10.1038/ncomms14572

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