Tumor resistance induced by syngeneic bone marrow transplantation and enhanced by interleukin 2: a model for the graft versus leukemia reaction.
Lethally irradiated C3H/HeN mice reconstituted with normal syngeneic bone marrow survived significantly longer than unmanipulated control mice following challenge with a lethal dose of 38C13 lymphoma cells 2 to 3 weeks post-bone marrow transplantation (BMT). Although the magnitude of this effect was modest, it was highly reproducible. This resistance-producing effect of BMT could be enhanced by interleukin 2 administration and could be abrogated by anti-asialo-GM1 antiserum treatment of recipients. These findings are consistent with the hypothesis that cells with a natural killer phenotype are activated by BMT and can mediate tumor resistance. These studies provide a model to explore the cellular basis, independent of donor alloreactivity, of the graft antitumor effect of BMT observed in humans.
Kwak
L W
LW
Department of Medicine, Stanford University Medical School, California 94305-5306.
Campbell
M J
MJ
Levy
R
R
D000818:Animals; D016026:Bone Marrow Transplantation; D005260:Female; D005677:G(M1) Ganglioside / Q000276:immunology; D007113:Immunity, Innate; D007116:Immunization, Passive; D007136:Immunoglobulins / Q000008:administration & dosage; D007376:Interleukin-2 / Q000627:therapeutic use*; D007694:Killer Cells, Natural / Q000276:immunology; D008213:Lymphocyte Activation; D016393:Lymphoma, B-Cell / Q000276:immunology* / Q000628:therapy; D051379:Mice; D008809:Mice, Inbred C3H; D014185:Transplantation, Isogeneic
D007136:Immunoglobulins; D007376:Interleukin-2; D005677:G(M1) Ganglioside; C018835:asialo GM1 ganglioside