THE EFFECTS OF PASSIVE ANTIVIRAL IMMUNOTHERAPY IN AKR MICE .2. SUSCEPTIBILITY TO B-CELL LYMPHOMAGENESIS

Prevention of high frequency spontaneous T cell lymphoma development i n AKR mice by mAb 18-5 treatment was shown to involve inhibition of th e recombinant Class I MCF virus formation and elimination of the early occurring potential lymphoma cells (PLCs). A low B cell lymphoma inci dence (16% at a mean latency of 540 days) and a low level of PLCs (yie lding 12% B cell lymphoma development following lymphoid cell transfer ) was observed in mAb 18-5 treated mice (in contrast to a high PLC lev el in thymectomized AKR mice that could he experimentally triggered to progress to overt CD5(+) B cell lymphomas). Administration of anti CD 8 mAb or IL-4 to 12-month-old mAb 18-5 pre-treated mice only slightly increased B cell lymphoma incidence (up to 30-40%). Exposure to split- dose irradiation resulted in 26% B cell lymphomas at a 250 day mean la tency. The phenotypes of the B lymphomas developing in mAb 18-5 treate d mice were: 8220(+) (14.8(+), 6B(2)(+)), 6C(3)(+), Mac-2(+), CD5(-). Most lymphomas expressed I-a and surface IgM, pointing to their mature B cell characteristics. Moreover, in some of the lymphomas, high leve ls of IgM production and secretion were determined. A comparison of th e morphological characteristics (based on light and ultrastructure mic roscopy) of CD5(+) and CD5(-) B cell lymphomas developing in AKR mice indicated marked differences, Analysis of the IgH locus of representat ive CD5(-) B lymphomas showed an identical pattern of IgH rearrangemen t in some tumors (similar to previous findings among CD5(+) lymphomas) . The virological analysis of the CD5(-) B cell lymphomas (similar to those observed in the CD5(+) B cell lymphomas of AKR origin) showed th at their development did not require formation of the pathogenic MCF r ecombinant viruses. The differences observed between the CD5(+) and CD 5(-) B cell lymphomas developing in AKR mice (following prevention of spontaneous T cell lymphomagenesis) may he due to their origin of diff erent B cell precursors or from B cells at different levels of differe ntiation.