دورية أكاديمية
أعرض في EDS

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

التفاصيل البيبلوغرافية
العنوان: Dendritic cell-mediated survival signals in Eμ-Myc B-cell lymphoma depend on the transcription factor C/EBPβ.
المؤلفون: Rehm A; 1] Department of Hematology, Oncology and Tumorimmunology, Max-Delbrück-Center for Molecular Medicine, MDC, 13125 Berlin, Germany [2] Department of Hematology and Oncology, Charité-Universitätsmedizin Berlin, Campus Virchow-Klinikum, 13353 Berlin, Germany., Gätjen M; Department of Hematology, Oncology and Tumorimmunology, Max-Delbrück-Center for Molecular Medicine, MDC, 13125 Berlin, Germany., Gerlach K; Department of Hematology, Oncology and Tumorimmunology, Max-Delbrück-Center for Molecular Medicine, MDC, 13125 Berlin, Germany., Scholz F; Department of Tumor Genetics and Immunogenetics, Max-Delbrück-Center for Molecular Medicine, MDC, 13125 Berlin, Germany., Mensen A; 1] Department of Hematology, Oncology and Tumorimmunology, Max-Delbrück-Center for Molecular Medicine, MDC, 13125 Berlin, Germany [2]., Gloger M; Department of Hematology, Oncology and Tumorimmunology, Max-Delbrück-Center for Molecular Medicine, MDC, 13125 Berlin, Germany., Heinig K; Department of Tumor Genetics and Immunogenetics, Max-Delbrück-Center for Molecular Medicine, MDC, 13125 Berlin, Germany., Lamprecht B; Department of Hematology, Oncology and Tumorimmunology, Max-Delbrück-Center for Molecular Medicine, MDC, 13125 Berlin, Germany., Mathas S; 1] Department of Hematology, Oncology and Tumorimmunology, Max-Delbrück-Center for Molecular Medicine, MDC, 13125 Berlin, Germany [2] Department of Hematology and Oncology, Charité-Universitätsmedizin Berlin, Campus Virchow-Klinikum, 13353 Berlin, Germany., Bégay V; Department of Cell Differentiation and Tumorigenesis, Max-Delbrück-Center for Molecular Medicine, MDC, 13125 Berlin, Germany., Leutz A; Department of Cell Differentiation and Tumorigenesis, Max-Delbrück-Center for Molecular Medicine, MDC, 13125 Berlin, Germany., Lipp M; Department of Tumor Genetics and Immunogenetics, Max-Delbrück-Center for Molecular Medicine, MDC, 13125 Berlin, Germany., Dörken B; 1] Department of Hematology, Oncology and Tumorimmunology, Max-Delbrück-Center for Molecular Medicine, MDC, 13125 Berlin, Germany [2] Department of Hematology and Oncology, Charité-Universitätsmedizin Berlin, Campus Virchow-Klinikum, 13353 Berlin, Germany., Höpken UE; Department of Tumor Genetics and Immunogenetics, Max-Delbrück-Center for Molecular Medicine, MDC, 13125 Berlin, Germany.
المصدر: Nature communications [Nat Commun] 2014 Sep 30; Vol. 5, pp. 5057. Date of Electronic Publication: 2014 Sep 30.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Nature Pub. Group Country of Publication: England NLM ID: 101528555 Publication Model: Electronic Cited Medium: Internet ISSN: 2041-1723 (Electronic) Linking ISSN: 20411723 NLM ISO Abbreviation: Nat Commun Subsets: MEDLINE
أسماء مطبوعة: Original Publication: [London] : Nature Pub. Group
مواضيع طبية MeSH: CCAAT-Enhancer-Binding Protein-beta/*immunology , Dendritic Cells/*immunology , Lymphoma, B-Cell/*immunology , Oncogene Protein p55(v-myc)/*immunology, Animals ; CCAAT-Enhancer-Binding Protein-beta/genetics ; Cell Differentiation ; Cell Line, Tumor ; Cell Survival ; Dendritic Cells/cytology ; Humans ; Lymphoma, B-Cell/genetics ; Lymphoma, B-Cell/physiopathology ; Mice ; Mice, Inbred C57BL ; Oncogene Protein p55(v-myc)/genetics
مستخلص: 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.
المشرفين على المادة: 0 (CCAAT-Enhancer-Binding Protein-beta)
0 (Oncogene Protein p55(v-myc))
تواريخ الأحداث: Date Created: 20141001 Date Completed: 20151028 Latest Revision: 20210102
رمز التحديث: 20240829
DOI: 10.1038/ncomms6057
PMID: 25266931
قاعدة البيانات: MEDLINE
الوصف
تدمد:2041-1723
DOI:10.1038/ncomms6057