Enhancement of B7-1 (CD80) expression on B-lymphoma cells by irradiation.

Irradiation of A20.2J mouse B-lymphoma cells enhanced their antigen-presenting ability to induce interleukin-2 (IL-2) production by 42-6A T cells specific for ovalbumin (OVA)323-339/I-Ad. Irradiated and fixed A20.2J cells were more efficient antigen-presenting cells (APC) to present OVA323-339 peptide than the unirradiated and fixed cells. Irradiation selectively increased the expression of B7-1 molecules, but not of the major histocompatibility complex class II molecules, B7-2, lymphocyte function-associated antigen-1, or intracellular adhesion molecule-1. Irradiation of A20.2J cells with 100 Gy followed by overnight incubation was optimal for the enhancement of B7-1 expression. Anti-B7-1 monoclonal antibody inhibited the irradiation-induced enhancement of APC function. Irradiation of A20.2J cells induced the accumulation of B7-1 mRNA. Thus, it was concluded that the enhancement of APC function by irradiation was due to the up-regulation of B7-1 molecules through the accumulation of its mRNA. Although partial inhibition of protein synthesis has been shown to enhance the accumulation of B7-1 mRNA and its expression, irradiation did not decrease the protein synthesis in A20.2J cells. The incubation with irradiated A20.2J cells stimulated unirradiated A20.2J cells to increase B7-1 expression, suggesting that irradiation of A20.2J cells induced expression or secretion of some molecule(s) to enhance B7-1 expression.