Receptor mediated murine leukemogenesis: monoclonal antibody induced lymphoma cell growth arrest.

We have proposed a receptor-mediated leukemogenesis hypothesis wherein T lymphomas would be clones of T cells bearing mitogen-linked surface receptors specific for the envelope determinants of the inducing MuLV (Weissman and Baird 1977; McGrath and Weissman 1978, 1979). We have tested a wide range of murine thymic lymphomas induced by thymotropic retroviruses and have shown that these cells indeed bear surface receptors highly specific for the retrovirus envelope glycoproteins produced by these cells (McGrath et al. 1978a,b). Even closely related recombinant retroviruses bound less well than the autologous retroviruses (McGrath et al. 1978b, McGrath and Weissman 1979). That these retroviruses and their interactions with T lymphoma cell receptors might be involved in the pathogenesis of murine leukemia was suggested by two kinds of experiments: First, only the leukemogenic viral isolates bouJ?-d specifically to lymphoma cel1 receptors, while nonleukemogenic but closely related viral preparations bound less weIl or not at all (McGrath et al. 1978b, McGrath and Weissman 1979). Second, if one examined the distribution of receptor bearing cells in the thymus of a preleukemic AKR mouse, only T cells bearing cell surface receptors recognizing the inducing MuLV were capable of adoptive transfer of the leukemic state, whereas morphologically similar cells within the same thymus were not capable of leukernic proliferation in syngeneic hosts (McGrath and Weissman 1978, 1979). While the above described experimental results are consistent with the receptor-mediated leukemogenesis hypo thesis and in fact were necessary postulates of the hypothesis