Immunological aspects of B-cell derived tumors in humans and rodents.

Translocation of the c-myc protooncogene to an immunoglobulin locus is a rate-limiting step in the genesis of three B-cell derived tumors: Burkitt lymphoma (BL) in humans, mouse plasmocytoma (MPC) and rat immunocytoma (RIC). Its consequences have been best analysed in BL. They involve a non-immunological and an immunological component. The former acts by preventing the B-cell from leaving the cycling compartment and entering the resting stage when programmed to do so. The latter acts by the down-regulation of certain HLA class I polymorphic specificities, leukocyte adhesion molecules and Epstein-Barr virus (EBV) encoded proteins. Together, they contribute to the escape of the BL cell from the host immune response.--We have also described a non-clonogenic, non-tumorigenic "revertant" subline among five EBV-convertants of an originally highly tumorigenic, EBV-negative BL line. The other four convertants have remained highly tumorigenic. Suppression of the tumorigenicity is associated with a switch to a lymphoblastoid cell line (LCL)-like phenotype, accompanied by the appearance of several activation markers. It is suggested that the LCL-type immunoblast comes under the influence of host feed-back controls that normally contribute to the constancy of the B-cell pool.