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[Cancer Research 61, 5523-5528, July 15, 2001]
© 2001 American Association for Cancer Research

Immunology

Antimetastatic Effect of CpG DNA Mediated by Type I IFN1

Michael Hafner, Rainer Zawatzky, Christian Hirtreiter, Wim A. Buurman, Bernd Echtenacher, Thomas Hehlgans and Daniela N. Männel2

Departments of Pathology/Tumor Immunology [B. E., T. H., D. N. M.] and Hematology/Oncology [M. H., C. H.], University of Regensburg, 93042 Regensburg, Applied Tumor Virology [R. Z.], 69120 Heidelberg, Germany, and Department of Surgery, University of Maastricht, Maastricht NL 6229 ER, the Netherlands [W. A. B.]

The mechanisms involved in the antimetastatic effect of CpG-containing DNA were investigated in a mouse model of experimental metastasis. Tumor cell colony formation in lungs or livers of mice after i.v. inoculation with syngeneic fibrosarcoma or thymoma cells was determined. The i.v. injection of plasmid DNA or synthetic oligodeoxynucleotides (ODNs) containing unmethylated CpG motifs before tumor cell application strongly inhibited metastasis. Because synthetic CpG-ODN was not directly tumor cytotoxic, the target cells for this CpG-ODN effect were determined. The cytotoxic activity on standard natural killer (NK) targets as well as on fibrosarcoma cells of splenic NK cells and NKT cell-containing liver mononuclear cells derived from CpG-ODN-treated mice was strongly enhanced. Participation of NK/NKT cells in the CpG-induced antimetastatic effect was demonstrated by reduction of the antimetastatic effect in mice depleted of NK/NKT cells and ß2-microglobulin-deficient mice. Neutralization of interleukin 12, interleukin 18, or IFN-{gamma} did not interfere with the CpG-induced antimetastatic effect. However, in sera of CpG-ODN-treated mice, high levels of IFN-{alpha} were detected, and in IFN-{alpha}/ß receptor-deficient mice, the CpG-ODN-induced antimetastatic effect was strongly reduced. These data indicate that CpG-ODNs activate NK/NKT cells for antimetastatic activity indirectly via IFN-{alpha}/ß receptor activation. The exploitation of the stimulatory activity of CpG-ODN for the innate immune system might be a useful strategy for antimetastatic therapy.




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