Dendritic cell-mediated survival signals in Eμ-Myc B-cell lymphoma depend on the transcription factor C/EBPβ

Armin Rehm (), Marcel Gätjen, Kerstin Gerlach, Florian Scholz, Angela Mensen, Marleen Gloger, Kristina Heinig, Björn Lamprecht, Stephan Mathas, Valérie Bégay, Achim Leutz, Martin Lipp, Bernd Dörken and Uta E. Höpken ()
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Armin Rehm: Oncology and Tumorimmunology, Max-Delbrück-Center for Molecular Medicine, MDC
Marcel Gätjen: Oncology and Tumorimmunology, Max-Delbrück-Center for Molecular Medicine, MDC
Kerstin Gerlach: Oncology and Tumorimmunology, Max-Delbrück-Center for Molecular Medicine, MDC
Florian Scholz: Max-Delbrück-Center for Molecular Medicine, MDC
Angela Mensen: Oncology and Tumorimmunology, Max-Delbrück-Center for Molecular Medicine, MDC
Marleen Gloger: Oncology and Tumorimmunology, Max-Delbrück-Center for Molecular Medicine, MDC
Kristina Heinig: Max-Delbrück-Center for Molecular Medicine, MDC
Björn Lamprecht: Oncology and Tumorimmunology, Max-Delbrück-Center for Molecular Medicine, MDC
Stephan Mathas: Oncology and Tumorimmunology, Max-Delbrück-Center for Molecular Medicine, MDC
Valérie Bégay: Max-Delbrück-Center for Molecular Medicine, MDC
Achim Leutz: Max-Delbrück-Center for Molecular Medicine, MDC
Martin Lipp: Max-Delbrück-Center for Molecular Medicine, MDC
Bernd Dörken: Oncology and Tumorimmunology, Max-Delbrück-Center for Molecular Medicine, MDC
Uta E. Höpken: Max-Delbrück-Center for Molecular Medicine, MDC

Nature Communications, 2014, vol. 5, issue 1, 1-14

Abstract: Abstract The capacity of dendritic cells (DCs) to regulate tumour-specific adaptive immune responses depends on their proper differentiation and homing status. Whereas DC-associated tumour-promoting functions are linked to T-cell tolerance and formation of an inflammatory milieu, DC-mediated direct effects on tumour growth have remained unexplored. Here we show that deletion of DCs substantially delays progression of Myc-driven lymphomas. Lymphoma-exposed DCs upregulate immunomodulatory cytokines, growth factors and the CCAAT/enhancer-binding protein β (C/EBPβ). Moreover, Eμ-Myc lymphomas induce the preferential translation of the LAP/LAP* isoforms of C/EBPβ. C/EBPβ−/− DCs are unresponsive to lymphoma-associated cytokine changes and in contrast to wild-type DCs, they are unable to mediate enhanced Eμ-Myc lymphoma cell survival. Antigen-specific T-cell proliferation in lymphoma-bearing mice is impaired; however, this immune suppression is reverted by the DC-restricted deletion of C/EBPβ. Thus, we show that C/EBPβ-controlled DC functions are critical steps for the creation of a lymphoma growth-promoting and -immunosuppressive niche.

Date: 2014
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DOI: 10.1038/ncomms6057

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