PuSH - Publication Server of Helmholtz Zentrum München: DC-NK cell cross talk as a novel CD4⁺ T-cell-independent pathway for antitumor CTL induction.

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Adam, C. ; King, S. ; Allgeier, T. ; Braumüller, H.* ; Lüking, C. ; Mysliwietz, J. ; Kriegeskorte, A.K. ; Busch, D.H.* ; Röcken, M.* ; Mocikat, R.

DC-NK cell cross talk as a novel CD4⁺ T-cell-independent pathway for antitumor CTL induction.

Blood 106, 338-344 (2005)

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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 interferon- expression and involved priming endogenous DCs for interleukin-12 production. Our data suggest a novel pathway linking innate and adaptive immunity.

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