B cells sustain inflammation and predict response to immune checkpoint blockade in human melanoma

Johannes Griss (), Wolfgang Bauer, Christine Wagner, Martin Simon, Minyi Chen, Katharina Grabmeier-Pfistershammer, Margarita Maurer-Granofszky, Florian Roka, Thomas Penz, Christoph Bock, Gao Zhang, Meenhard Herlyn, Katharina Glatz, Heinz Läubli, Kirsten D. Mertz, Peter Petzelbauer, Thomas Wiesner, Markus Hartl, Winfried F. Pickl, Rajasekharan Somasundaram, Peter Steinberger and Stephan N. Wagner ()
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Johannes Griss: Medical University of Vienna
Wolfgang Bauer: Medical University of Vienna
Christine Wagner: Medical University of Vienna
Martin Simon: Medical University of Vienna
Minyi Chen: Medical University of Vienna
Katharina Grabmeier-Pfistershammer: Medical University of Vienna
Margarita Maurer-Granofszky: Medical University of Vienna
Florian Roka: Medical University of Vienna
Thomas Penz: CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences
Christoph Bock: CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences
Gao Zhang: The Wistar Institute
Meenhard Herlyn: The Wistar Institute
Katharina Glatz: University Hospital Basel
Heinz Läubli: University Hospital Basel
Kirsten D. Mertz: Cantonal Hospital Baselland
Peter Petzelbauer: Medical University of Vienna
Thomas Wiesner: Medical University of Vienna
Markus Hartl: University of Vienna, Vienna BioCenter (VBC)
Winfried F. Pickl: Infectiology and Immunology, Medical University of Vienna
Rajasekharan Somasundaram: The Wistar Institute
Peter Steinberger: Institute of Immunology, Center for Pathophysiology, Infectiology and Immunology, Medical University of Vienna
Stephan N. Wagner: Medical University of Vienna

Nature Communications, 2019, vol. 10, issue 1, 1-14

Abstract: Abstract Tumor associated inflammation predicts response to immune checkpoint blockade in human melanoma. Current theories on regulation of inflammation center on anti-tumor T cell responses. Here we show that tumor associated B cells are vital to melanoma associated inflammation. Human B cells express pro- and anti-inflammatory factors and differentiate into plasmablast-like cells when exposed to autologous melanoma secretomes in vitro. This plasmablast-like phenotype can be reconciled in human melanomas where plasmablast-like cells also express T cell-recruiting chemokines CCL3, CCL4, CCL5. Depletion of B cells in melanoma patients by anti-CD20 immunotherapy decreases tumor associated inflammation and CD8+ T cell numbers. Plasmablast-like cells also increase PD-1+ T cell activation through anti-PD-1 blockade in vitro and their frequency in pretherapy melanomas predicts response and survival to immune checkpoint blockade. Tumor associated B cells therefore orchestrate and sustain melanoma inflammation and may represent a predictor for survival and response to immune checkpoint blockade therapy.

Date: 2019
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DOI: 10.1038/s41467-019-12160-2

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