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The CXC Chemokines IP-10 and Mig Are Necessary for IL-12-Mediated Regression of the Mouse RENCA Tumor¹

Charles S. Tannenbaum^2,*, Raymond Tubbs^*,, David Armstrong^*, James H. Finke^*, Ronald M. Bukowski^*, and Thomas A. Hamilton^*

^* Department of Immunology, Lerner Research Institute; and Departments of Hematology-Oncology and Anatomic Pathology, Cleveland Clinic Foundation, Cleveland, OH 44195

The role of the non-ELR-containing CXC chemokines IP-10 and Mig in antitumor activity induced by systemic treatment with IL-12 was examined in mice bearing the murine renal adenocarcinoma RENCA. IL-12 treatment produces a potent antitumor effect that is associated with tumor infiltration by CD8⁺ T lymphocytes. The regression of tumor is associated with the elevated expression of the IFN--inducible chemokines IP-10 and Mig within the tumor tissue. IP-10 and Mig have been shown to function as chemoattractants for activated T lymphocytes. In animals treated with rabbit polyclonal Abs specific for IP-10 and for Mig, the IL-12-induced regression of RENCA tumors was partially abrogated. This effect was associated with a dramatic inhibition of T cell infiltration. Thus, it appears that IL-12-dependent, T cell-mediated antitumor activity requires the intermediate expression of IP-10 and Mig to recruit antitumor effector T cells to the tumor site.