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Blood, 1 July 2005, Vol. 106, No. 1, pp. 338-344. Prepublished online as a Blood First Edition Paper on March 15, 2005; DOI 10.1182/blood-2004-09-3775. This Article Full Text Full Text (PDF) All Versions of this Article: 2004-09-3775v1 106/1/338    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 Adam, C. Articles by Mocikat, R. Search for Related Content PubMed PubMed Citation Articles by Adam, C. Articles by Mocikat, R. Related Collections Immunobiology Neoplasia Immunotherapy Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA DC-NK cell cross talk as a novel CD4+ T-cell–independent pathway for antitumor CTL induction Christian Adam, Susan King, Thomas Allgeier, Heidi Braumüller, Carolin Lüking, Josef Mysliwietz, Anja Kriegeskorte, Dirk H. Busch, Martin Röcken, and Ralph Mocikat From the GSF–Institut für Molekulare Immunologie, Munich, Germany; the Universitäts-Hautklinik, Universitätsklinikum Tübingen, Eberhard-Karls-Universität, Tübingen, Germany; and the Institut für Medizinische Mikrobiologie, Immunologie und Hygiene, Technische Universität, Munich, Germany. It is generally accepted that priming of antitumor CD8+ cytotoxic T lymphocytes (CTLs) needs help that can be provided by CD4+ T cells. We show that interactions between dendritic cells (DCs) and natural killer (NK) cells can bypass the T helper arm in CTL induction. Bone marrow–derived DCs caused rejection of the A20 lymphoma and induced tumor-specific long-term memory, although they were not loaded with tumor-derived antigen. Experiments using CD40- knock-out mice and cell depletion showed that this effect did not require CD4+ cells. Both primary rejection and long-term CTL memory were the result of NK cell activation by DCs. NK cytotoxicity, which was necessary for primary rejection, was dependent on expression of natural killer group 2 D (NKG2D) ligands on tumor cells. Blocking of these ligands using NKG2D tetramers abrogated tumor killing in vitro and in vivo. The long-term response was due to CTLs directed against antigen(s) expressed on A20 and in vitro–differentiated DCs. The mechanism leading to CD4+ helper cell–independent CTL responses was elucidated as a cascade that was initiated by NK cell activation. This pathway was dependent on inter-feron- expression and involved priming endogenous DCs for interleukin-12 production. 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