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Blood, 1 July 2005, Vol. 106, No. 1, pp. 175-183. Prepublished online as a Blood First Edition Paper on March 8, 2005; DOI 10.1182/blood-2004-08-3072. This Article Full Text Full Text (PDF) Supplemental Data All Versions of this Article: 2004-08-3072v1 106/1/175    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Kriehuber, E. Articles by Maurer, D. Search for Related Content PubMed PubMed Citation Articles by Kriehuber, E. Articles by Maurer, D. Related Collections Immunobiology Phagocytes Apoptosis Signal Transduction Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Balance between NF-B and JNK/AP-1 activity controls dendritic cell life and death Ernst Kriehuber, Wolfgang Bauer, Anne-Sophie Charbonnier, Dorian Winter, Stefan Amatschek, Dietmar Tamandl, Norbert Schweifer, Georg Stingl, and Dieter Maurer From the Department of Dermatology, Division of Immunology, Allergy and Infectious Diseases, Medical University of Vienna, Austria; the Center of Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria; the Department of Surgery, Medical University of Vienna, Austria; and the Department of Lead Discovery, Boehringer Ingelheim Austria, Vienna, Austria. The life cycle of dendritic cells (DCs) must be precisely regulated for proper functioning of adaptive immunity. However, signaling pathways actively mediating DC death remain enigmatic. Here we describe a novel mechanism of hierarchical transcriptional control of DC life and death. Ligation of tumor necrosis factor receptor superfamily (TNFR-SF) members on DCs and cognate contact with T cells resulted in quantitatively balanced nuclear factor-B (NF-B) and c-Jun N-terminal kinase (JNK)–mediated activator protein-1 (AP-1) induction and strongly enhanced DC longevity. Specific blockade of NF-B in DCs induced strongly augmented JNK/AP-1 activity because of elevated levels of reactive oxygen species. In this scenario, DC activation by TNFR-SF members or T cells induced DC apoptosis. Specific inhibition of JNK/AP-1 rescued DCs from this activation-induced cell death program and restored TNFR-SF member- and T-cell–mediated survival. We conclude that JNK/AP-1 activity is under negative feedback control of NF-B and can execute apoptosis in DCs. Thus, feedback-controlled signaling amplitudes of 2 transcriptional pathways decide the fate of a DC. 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