Prevention of spontaneous AKR T cell lymphomagenesis by elimination of potential lymphoma cells with antibody to specific gp 71 determinants.
AKR mice, highly susceptible to spontaneous T cell lymphomagenesis, were protected from developing the disease by a course of daily treatment with antibody 18-5 to gp 71 determinants (administered from birth to 10 days). Potential lymphoma cells (PLC) identified among bone marrow cells of untreated AKR mice since birth (using the transplantation bioassay method) were eliminated following treatment with antibody 18-5. Namely, transplantation of bone marrow cells and thymocytes of 250-day-old untreated AKR mice into (AKR/J x DBA/2)F1 and/or AKR recipients yielded 86-93% T cell lymphoma of AKR origin at a short mean latent period of 38-42 days. In contrast, transfer of lymphoid cells from 18-5-treated mice at a matching age caused only 7-13% T cell lymphoma of AKR origin. The accelerating effect of MCF 247 on lymphoma development in untreated AKR mice was not effective in 18-5-treated mice, probably due to lack of PLC that are promoted by MCF 247 to overt T cell lymphoma. The characteristic changes in thymus subpopulations preceding lymphoma development and coinciding with PLC identification in the thymus of untreated mice was prevented by 18-5. It is suggested that prevention of lymphoma development in AKR mice by passive antiviral immunotherapy involves elimination of PLC representing the initial tumorigenic phase in AKR lymphomagenesis.
Haran-Ghera
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N
Department of Chemical Immunology, Weizmann Institute of Science, Rehovot, Israel.
Peled
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A
D000375:Aging; D000818:Animals; D000911:Antibodies, Monoclonal / Q000494:pharmacology; D000918:Antibody Specificity; D006023:Glycoproteins / Q000276:immunology*; D007519:Isoantigens / Q000276:immunology; D016399:Lymphoma, T-Cell / Q000517:prevention & control*; D051379:Mice; D008806:Mice, Inbred AKR; D009858:Oncogenic Viruses / Q000276:immunology*
D000911:Antibodies, Monoclonal; D006023:Glycoproteins; D007519:Isoantigens