Immunological mechanisms in the pathogenesis of virus‐induced murine leukemia. I. Autoreactivity

Abstract

By an in vitro microcytotoxicity assay, thymocytes from mice infected with Moloney murine leukemia virus since birth (MuLV-M carriers) caused a dramatic reduction of normal, non-infected syngeneic target cells; they usually spared identically derived target cells infected with MuLV-M. Thymocytes from normal mice slightly stimulated the replication of the same target cells. This pattern of carrier thymocyte reactivity was evident at all ages tested during both preneoplastic and neoplastic periods. Transplantable lymphoma cells derived from a carrier mouse with overt thymic lymphoma behaved similarly. Lymphocytes from the spleens and lymph nodes of young preleukemic carriers (8–12 weeks old) usually were reactive against MuLV-M-infected target cells and not against non-infected target cells. In contrast, lymphocytes from older preleukemic carriers (16–17 weeks old) reacted in a manner similar to carrier thymocytes. These observations suggest that the thymic lymphoma induced by MuLV-M may result in part from an autoreactive process originating in the thymus, but eventually spreading to the peripheral lymphoid tissues.