V-rel and C-rel Modulate the Expression of Both Bursal and Non-Bursal Antigens on Avian B-Cell Lymphomas

Abstract

Infection of chickens with the avian retrovirus, Reticuloendotheliosis virus-T [REV-T(CSV)], results in the rapid development of a variety of hematopoietic tumors [2, 4]. Typically, the birds die between 1 and 2 weeks bearing pauciclonal tumors with extensive metastatic disease. Examination of cell surface lineage specific markers demonstrates that these tumors can be derived from B-cells, T-cells and cells within the myeloid lineage [1,3]. Genetic experiments have demonstrated that tumor development results from the expression of the viral oncogene, v-rel [5, 6]. V-rel is related to the proteins p50 and p65 that comprise the transcriptional complex NF-kB [7, 17, 18, 21]. Extensive analysis has demonstrated that this complex regulates transcription through the formation of heterodimers that bind DNA [15, 22]. Transcriptional regulation of a number of proteins may be regulated in part through the interaction of NF-kB protein with NF-kB consensus sequence in the promoter region of these genes [7, 15]. Transcription would appear to be activated by external signals that interact with cell surface receptors and result in the conversion of NF-kB from a cytoplasmic protein complex to a nuclear complex that can bind DNA [16].