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Antilymphoma Activity of Human T-Cells in Mice with Severe Combined Immune Deficiency¹

Department of Medicine [V. M., F. K. C., N. A.], University of Wisconsin Clinical Cancer Center [V. M., B. E. S., R. H.], and the Department of Pediatrics [R. H.] of the University of Wisconsin, Madison, Wisconsin 53792

Human Burkitt lymphoma (Daudi) cells grow as disseminated tumors in mice with severe combined immune deficiency (SCID) after either i.v. or i.p. injection. These cells are lysed in vitro by human V9/V2 T-cells that recognize the groEL homologue on the Daudi cell surface. We report that both Daudi cell-stimulated peripheral blood mononuclear cells (Daudi-PBMC) containing 41-95% of V9/V2 T-cells and V9/V2 T-cell clones prolong the survival of SCID mice given inoculations of a lethal dose of Daudi cells. Groups of 6–8-week-old SCID mice were given inoculations i.v. or i.p. of 10⁵ Daudi cells followed (through different injection sites) by: (a) 10⁷ Daudi-PBMC; or (b) 10⁷ unstimulated PBMC; or (c) 0.9% saline solution. All animals in groups (b) and (c) died of disseminated lymphoma, and their survival was significantly shorter than that of mice in group (a) (P < 0.001 for both i.v. and i.p. routes). Significant antitumor effects were also detected when Daudi-PBMC were injected 4 days before or 4 days after Daudi cells (P < 0.05). In vivo depletion of murine natural killer cells by anti-asialo GM-1 rabbit antiserum did not affect survival, suggesting that these cells did not contribute to lymphoma killing. Daudi-PBMC did not exert in vivo antitumor activity against the control Raji lymphoma. Mice receiving i.p. injections of Daudi cells followed by cytotoxic V9/V2 T-cell clones also survived significantly longer (P < 0.05 for 3 different clones) than animals given Daudi cells alone or Daudi cells followed by noncytotoxic T-cell clones. Our results indicate that this model system can be used for studies of human antilymphoma T-cell responses in vivo.

¹ This work was supported by Grant 1RG-35-32-12 awarded by the American Cancer Society and by University of Wisconsin Medical School and Graduate School grants.

² To whom requests for reprints should be addressed, at H4/546 Clinical Sciences Center, 600 Highland Avenue, Madison, WI 53792.

Received 11/11/91. Accepted 8/ 5/92.

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