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Cell-Mediated Immunity to Friend Virus-Induced Leukemia

III. Characteristics of Secondary Cell-Mediated Cytotoxic Response¹

From the Laboratory of Immunodiagnosis, National Cancer Institute, Bethesda, Maryland 20014, and Litton-Bionetics, Inc., Kensington, Maryland 20795

Abstract

By employing the ¹²⁵IUdR release cytotoxicity assay, we have been able to measure the primary and secondary cell-mediated cytotoxic response of C57BL/6 mice to FBL-3 cells, a syngeneic Friend virus-induced leukemia. It was found that the secondary cell-mediated cytotoxic response occurred more rapidly after challenge (within 3 days) than the primary response, and the levels of reactivity were considerably higher. As in the primary response, the secondary cytotoxic reactivity of spleen cells was T cell dependent, being eliminated by pretreatment with anti- antibody plus complement. However, the secondary reactivity of pertioneal exudate (PE) cells was not entirely T-cell dependent. The specificity of the secondary cytotoxic response was analyzed by primary or secondary immunization with various tumor cells and by testing of cytotoxic lymphocytes against a variety of target cells. When spleen cells were used for testing, only tumor cells induced by Friend, Moloney, or Rauscher (FMR) leukemia viruses could produce secondary cell-mediated cytotoxic responses against FBL-3 cells. This correlated well with the specificity observed in the in vivo tumor transplantation protection studies. Similarly, spleen cells immune to FBL-3 had appreciable cytotoxicity against tumor cells induced by FMR viruses. The FBL-3 immune mice also gave significant protection against the challenge of FMR leukemias. When PE cells were used for testing, they gave a broader spectrum of reactivity. These cells usually gave higher levels of cytotoxicity against tumor cells induced by FMR viruses, but also gave less, but appreciable, cytotoxicity against non-FMR tumors. The latter reactivity might be related to the antigens induced by the murine endogenous type C viruses.

Footnotes

¹ This work is supported in part by Contract NIH-NCI-G-72-3878 with Litton Bionetics, Inc., 5516 Nicholson Lane, Kensington, Maryland 20795.

² Laboratory of Immunodiagnosis, National Cancer Institute, Bethesda, Maryland 20014.

³ Present address: Laboratory of Cell Biology, National Cancer Institute, Bethesda, Maryland 20014. Please send correspondence to Dr. Chou-Chik Ting, National Cancer Institute, Bldg. 8, Room 219, Bethesda, Maryland 20014.

⁴ Litton-Bionetics, Inc., 5516 Nicholson Lane, Kensington, Maryland 20795.

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