Receptor mediated leukemogenesis: murine leukemia virus interacts with BCL1 lymphoma cell surface IgM.

Murine leukemia virus (MuLV) induced T-lymphomas bear surface receptors specific for the leukemogenic retroviruses they produce. We have proposed that such virus receptors on lymphoid tumors are the antigen-specific receptors present on their normal lymphocyte counterparts. To determine the relationship between immune receptors and virus receptors on malignant lymphocytes, a spontaneous B cell lymphoma, BCL1, was investigated. BCL1-lymphoma cells from an in vivo passaged BCL1-cell line grew in vitro only in contact with splenic stromal cells. These stromal cells produced a retrovirus, termed BCL1-V, which was lymphotropic but not leukemogenic. BCL1 cells bound BCL1-V, whereas normal spleen cells did not. Isolated BCL1-IgM bound BCL1-V, whereas three other IgM myeloma proteins, MOPC-104E, CBPC-112, and HPC-76, did not. Rat anti-BCL1-IgM monoclonal antibodies recognizing mu chain isotypic determinants and BCL1-specific idiotypic specificities, blocked BCL1-V binding to BCL1 IgM. These data support the receptor mediated leukemogenesis hypothesis, suggest a role for virus:cell surface immunoglobulin interactions in the development of B cell lymphoma, and implicate an antigen presenting cell population in the lymphomagenic process.