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A Role for IFN- in Primary and Secondary Immunity Generated by NK Cell-Sensitive Tumor-Expressing CD80 In Vivo¹

Janice M. Kelly^*, Kazuyoshi Takeda, Phillip K. Darcy^*, Hideo Yagita and Mark J. Smyth^2,*

^* Cancer Immunology Program, Sir Donald and Lady Trescowthick Laboratories, Peter MacCallum Cancer Institute, East Melbourne, Victoria, Australia; and Department of Immunology, Juntendo University School of Medicine, Bunkyo-ku, Tokyo, Japan

We have investigated the primary and secondary immunity generated in vivo by a MHC class I-deficient tumor cell line that expressed CD80 (B7-1). CD80 expression enhanced primary NK cell-mediated tumor rejection in vivo and T cell immunity against secondary tumor challenge. CD80 expression enhanced primary NK cell-mediated tumor rejection, and both NK cell perforin and IFN- activity were critical for the rejection of MHC class I-deficient RMA-S-CD80 tumor cells. This primary rejection process stimulated the subsequent development of specific CTL and Th1 responses against Ags expressed by the MHC class I-deficient RMA-S tumor cells. The development of effective secondary T cell immunity could be elicited by irradiated RMA-S-CD80 tumor cells and was dependent upon NK cells and IFN- in the priming response. Our findings demonstrate a key role for IFN- in innate and adaptive immunity triggered by CD80 expression on tumor cells.

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