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Genome-Wide Analysis of Molecular Changes in IL-12-Induced Control of Mammary Carcinoma via IFN--Independent Mechanisms¹

Department of Microbiology and Immunology, Weill Medical College of Cornell University, New York, NY 10021

IL-12 is a major activator of tumor-killing NK cells and CTL. IFN- mediates most of the well-known immunological activities of IL-12. In this study, we report IFN--independent activities induced by therapeutic application of rIL-12 in restricting tumor growth and metastasis in the 4T1 murine mammary carcinoma model. IFN--deficient mice carrying 4T1 tumor exhibit no gross defect in the number of tumor-infiltrating lymphocytes but have exaggerated angiogenesis in the tumor. Administration of IL-12 is able to constrict blood vessels in the tumor in the absence of IFN-, and retains certain therapeutic efficacy even when applied late during tumor progression. IL-12 exposure in vivo does not irreversibly alter the immunogenicity of the tumor. Finally, global gene expression analysis of primary tumors reveals IL-12-induced molecular patterns and changes, implicating a number of novel genes potentially important for IFN--independent immune responses against the tumor, for IL-12-mediated antiproliferation, antimetastasis, and antiangiogenesis activities.

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The JI 2004 172: 3981-3982. [Full Text]  

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