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Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, Maryland 20014 [L. E., D. H. K., I. G., W. E. P.], and Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115 [B. B.]
The protection of adult strain 2 guinea pigs challenged with lethal L2C leukemia as a result of prior administration of immunocompetent allogeneic lymphoid cells has been shown to result from the development of the graft-versus-host reaction. The concomitant existence of a host rejection response is not required as evidenced by the capacity to protect against leukemia by passive transfer of parental strain 2 or strain 13 lymphoid cells in 2 x 13 F1 recipients. The possibility that protection results from direct rejection, by donor cells, of the L2C leukemia on the basis of an immune response directed against strain 2 histocompatibility antigens present on L2C cells is definitively excluded, since strain 2 parental cells are equivalent to strain 13 cells in affording protection to F1 recipients. We suggest that immunocompetent lymphoid cells of the host may exert the primary effector mechanism in this phenomenon, although a role for cells of the reticuloendothelial system has not been excluded. A model for immunotherapy of guinea pigs with already existent leukemia utilizing repeated allogeneic cell transfers was shown to be effective in significantly prolonging survival of such recipients. The potential promise of such an approach to immunotherapy of human cancers is considered.
1 Present address: Department of Medicine, Barnes Hospital, St. Louis, Mo. 63110.
2 To whom reprint requests should be addressed. Present address: Department of Pathology, Harvard Medical School, Boston, Mass. 02115.
Received 7/ 8/71. Accepted 9/15/71.
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