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Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, Maryland 20014 [D. H. K., L. E., W. E. P., I. G.], and Department of Pathology, Harvard Medical School, Boston,Massachusetts 02115 [B. B.]
The passive transfer of immunocompetent lymphoid cells from allogeneic strain 13 guinea pigs to normal adult strain 2 recipients which are subsequently challenged with a lethal inoculum of L2 C leukemia significantly alters the development of systemic leukemia in such recipients. This is manifested by striking prolongation of survival times in all allogeneic cell recipients even when doses of L2 C as much as 30-fold higher than the uniformly lethal dose are used. Furthermore, in 21% of all cases long-term protection against development of leukemia has been observed. The temporal relationship between cell transfer and leukemic challenge was shown to be crucial, and the antileukemic protective effect was observed even at a time when all donor cells had presumably been rejected. The primary involvement of host immune mechanisms in this antileukemia protection phenomenon is further suggested by the ability of 50% of allogeneic cell recipients subjected to a second leukemic challenge to reject this lethal L2 C inoculum. We suggest that this protective phenomenon most likely reflects critical cellular actions performed by the host cell population which has been highly stimulated by events related to the graft-versus-host reaction. The possible host cell types serving as primary effectors are discussed.
1 To whom requests for reprints should be addressed. Present address: Department of Pathology, Harvard Medical School, Boston, Mass. 02115.
2 Present address: Department of Medicine, Barnes Hospital, St. Louis, Mo. 63110.
Received 7/ 8/71. Accepted 9/15/71.
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