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Laboratory of Cellular Immunology, Flemish Institute for Biotechnology, Free University of Brussels, IMOL II, Paardenstraat 65, Sint Genesius Rode, 1640 [A. B. G., G. R., P. D.], and Laboratory of Physiology, Medical School, Free University of Brussels, Jette, 1090 [M. B., S. D., K. T.], Belgium
The interaction between B7-1 and CD28 provides costimulatory signals not only for T cells but also for natural killer (NK) cells. Highly metastatic mouse T lymphoma cells (BW-Li) can escape from NK cell-mediated killing by expressing H-2Dk molecules that negatively regulate NK lytic activity. We have analyzed whether B7-1:CD28 overrules the MHC class I-mediated inactivation of NK cells by transfecting BW-Li with the gene coding for B7-1. Expression of B7-1 rendered BW-Li cells sensitive toward NK cells. The experimental metastatic capacity of the B7-1 transfectants was drastically reduced in both syngeneic AKR and SCID mice but could be restored in SCID-bg mice. These results provide direct evidence that B7-1 expression leads to NK-mediated elimination of metastasizing, NK-resistant tumor cells.
1 This investigation was supported by grants from the GOA (P. D., K. T.) and the Governmental Vlaams Actieprogramma Biotechnologie (P. D.). P. D. is a research director of the Nationaal Fonds voor Wetenschappelijk Onderzoek (NFWO). S. D. holds a fellowship of the Vlaams Instituut voor de bevordering van het wetenschappelijk-technologisch onderzoek in de industrie. M. B. is a senior research assistant of the NFWO, and G. R. is a research assistant of the NFWO.
2 To whom requests for reprints should be addressed.
Received 3/29/95. Accepted 5/18/95.
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