PD-L1 is expressed on human platelets and is affected by immune checkpoint therapy
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Verena Rolfes1,*, Christian Idel2,*, Ralph Pries2,*, Kirstin Plötze-Martin2, Jens Habermann3, Timo Gemoll3, Sabine Bohnet4, Eicke Latz1,5,6, Julika Ribbat-Idel7, Bernardo S. Franklin1,* and Barbara Wollenberg2,*
1Institute of Innate Immunity, University Hospital, University of Bonn, Bonn, Germany
2University Hospital Schleswig Holstein, Campus Lübeck, Clinic for Otorhinolaryngology – Head and Neck Surgery, Luebeck, Germany
3University Hospital Schleswig Holstein, Campus Lübeck, Section for Translational Oncology and Biobanking, Clinic for Surgery, Luebeck, Germany
4University Hospital Schleswig Holstein, Campus Lübeck, Clinic for Pulmonary Medicine, Luebeck, Germany
5Department of Infectious Diseases and Immunology, University of Massachusetts Medical School, Worcester, MA, USA
6German Center for Neurodegenerative Diseases, Bonn, Germany
7Department of Pathology, University Medical Center Schleswig-Holstein, Luebeck, Germany
*These authors have contributed equally to this work
Barbara Wollenberg, email: Barbara.Wollenberg@uksh.de
Bernardo S. Franklin, email: firstname.lastname@example.org
Keywords: head and neck cancer; biomarkers for PD1-PD-L1 checkpoint therapy; tumor-educated platelets; atezolizumab
Received: March 07, 2018 Accepted: April 28, 2018 Published: June 08, 2018
Cancer immunotherapy has been revolutionised by drugs that enhance the ability of the immune system to detect and fight tumors. Immune checkpoint therapies that target the programmed death-1 receptor (PD-1), or its ligand (PD-L1) have shown unprecedented rates of durable clinical responses in patients with various cancer types. However, there is still a large fraction of patients that do not respond to checkpoint inhibitors, and the challenge remains to find cellular and molecular cues that could predict which patients would benefit from these therapies. Using a series of qualitative and quantitative methods we show here that PBMCs and platelets from smokers and patients with head and neck squamous cell carcinoma (HNSCC) or lung cancer express and up-regulate PD-L1 independently of tumor stage. Furthermore, treatment with Atezolizumab, a fully humanised monoclonal antibody against PD-L1, in 4 patients with lung cancer caused a decrease in PD-L1 expression in platelets, which was restored over 20 days. Altogether, our findings reveal the expression of the main therapeutic target in current checkpoint therapies in human platelets and highlight their potential as biomarkers to predict successful therapeutic outcomes.
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