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Mediation of Immunity to Tumor-specific Transplantation Antigens by RNA Inhibition of Isograft Growth in Rats

Surgery Branch, National Cancer Institute, NIH, Bethesda, Maryland 20014

Inbred · Fischer 344/N rats were immunized to a benz(a)pyrene-induced Fischer 344/N sarcoma (BP-1R) by the excision of growing tumor transplants. This tumor contained tumor-specific transplantation antigens; spleen cells from rats immunized to this tumor adoptively transferred tumor-specific transplantation immunity to syngeneic, normal recipients. RNA-rich extracts were prepared from the spleens of immunized rats. Normal, nonimmune, syngeneic spleen cells were incubated in vitro with these preparations of "BP-1R-immune" RNA and injected i.v. into Fischer 344/N rats daily for 3 days. The growth of BP-1R isografts in rats inoculated 24 hr after the 3rd injection of these RNA-treated spleen cells was significantly inhibited when compared to recipients of syngeneic spleen cells preincubated with RNA from the spleens of unimmunized Fischer 344/N rats or to untreated controls (no spleen cells). In a similar, but not identical, experiment, BP-1R isografts were inoculated synchronous with the 1st of 3 daily injections of syngeneic spleen cells preincubated with BP-1R-immune RNA. Significant reduction in the incidence of tumor isograft development was noted in recipients of these RNA-treated spleen cells when compared to recipients of untreated Fischer 344/N spleen cells or to untreated controls. Treatment of the active immune RNA preparations with RNase resulted in their complete inactivation.

¹ Trainee in Academic Surgery, Boston University School of Medicine, University Hospital, Boston, Mass. 02118.

² Medical Investigator, Veterans Administration Hospital, Sepulveda, Calif. 91343; Assistant Professor of Surgery and Oncology, Surgical Service, UCLA School of Medicine, Los Angeles, Calif, 90052.

Received 8/12/71. Accepted 1/12/72.