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

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  • Armin Rehm

    (Oncology and Tumorimmunology, Max-Delbrück-Center for Molecular Medicine, MDC
    Charité-Universitätsmedizin Berlin, Campus Virchow-Klinikum)

  • 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
    Present address: Charité-Universitätsmedizin Berlin, Institute for Medical Immunology, 13353 Berlin, Germany)

  • 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
    Charité-Universitätsmedizin Berlin, Campus Virchow-Klinikum)

  • 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
    Charité-Universitätsmedizin Berlin, Campus Virchow-Klinikum)

  • Uta E. Höpken

    (Max-Delbrück-Center for Molecular Medicine, MDC)

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.

Suggested Citation

  • 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 , 2014. "Dendritic cell-mediated survival signals in Eμ-Myc B-cell lymphoma depend on the transcription factor C/EBPβ," Nature Communications, Nature, vol. 5(1), pages 1-14, December.
    • Handle: RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms6057
    DOI: 10.1038/ncomms6057
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