IMMUNOPATHOLOGY OF B-CELL LYMPHOMAS INDUCED IN C57BL/6 MICE BY DUALTROPIC MURINE LEUKEMIA-VIRUS (MULV)

  • 1 January 1982
    • journal article
    • research article
    • Vol. 107  (3) , 362-377
Abstract
Combined clinicopathologic and immunomorphologic evidence is presented that a murine leukemia virus (MuLV) with the dualtropic host range (dualtropic radiation leukemia virus [RadLV]) is capable of producing a clinically malignant lesion composed of immunoblasts and associated plasma cells in C57BL/6 mice. This process, morphologically diagnosed as an immunoblastic lymphoma of B cells using standard histopathologic criteria, was distinctly polyclonal with regard to Ig isotype when analyzed for both surface and cytoplasmic Ig. This clinicopathologically malignant, dualtropic MuLV-induced, polyclonal immunoblastic lymphoma of B cells in C57BL/6 mice was normal diploid and unable to be successfully transplanted to nonimmunosuppressed syngeneic recipients. Although all serum H and L chain components were progressively elevated as the tumor load increased, the polyclonal increase in serum Ig was most pronounced for .mu. H and .kappa. L chains (i.e., .mu. > .gamma.2A > .alpha. > .gamma.2B > .gamma.1; k > .lambda.). The dissociation of clinicopathologic and biologic criteria for malignancy in the presently described dualtropic RadLv-induced B cell lesion is sharply contrasted with the thymotropic RadLV-induced T cell lymphoblastic lymphoma in C57BL/6 mice. This process is also a clinicopathologically malignant lesion but, based on biologic criteria, is distinctly monoclonal, aneuploid and easily transplanted to nonimmunosuppressed syngeneic recipients. The close clinicopathologic and biologic similarities of the dualtropic MuLV-induced animal model to corresponding human B cell lymphoproliferative diseases are stressed.