The Journal of Immunology, Vol 155, Issue 10 4783-4789, Copyright © 1995 by American Association of Immunologists

ARTICLES

Expression of activated H-rasval12 in nontumorigenic and non-cross- reactive syngeneic cells induces tumor antigens cross-reactive with rat mammary adenocarcinoma 13762

AB Frey and S Cestari
Department of Cell Biology, New York University Medical Center, NY 10016, USA.

Adenocarcinoma 13762 expresses tumor Ags that can induce protective immunity to tumorigenic challenge. Syngeneic fibroblast Rat1 cells transformed by expression of H-rasval12 (Rat1/ras) but not parental Rat1 cells, and p53-transformed Rat1 cells, or other syngeneic cells or tumors, can immunize rats against tumorigenic challenge of 13762 tumor. Coincident with induced resistance to 13762 tumors, immunization of rats with Rat1/ras tumor induces CD4+ T cells that cross-react with adenocarcinoma 13762 in vitro and transfer protective immunity to tumorigenic 13762 challenge in vivo. Cross-reactive tumor Ags expressed in Rat1/ras tumor are not derived from ras protein, because immunization with purified H-rasval12 protein induces protective immunity to challenge by Rat1/ras tumor but not to adenocarcinoma 13762. In addition, immunization with H-rasval12 protein induces anti- ras CD4+ T cells that are uniquely reactive with Rat1/ras tumor: anti- ras T cells are not reactive with 13762 tumor in vitro and do not confer protective immunity to challenge with 13762 tumor in vivo. Tumor Ags expressed in Ras-transformed Rat1 cells that elicit cross- protective immunity likely arise as a consequence of transformation mediated by activated ras oncogene but are not derived from the Ras protein sequence.