[Function of B7/CD28 in anti-myeloma immunoreaction through activating T cells]

To explore the role of B7/CD28 molecule in priming the anti-myeloma effect of T lymphocyte and the mechanism by which CD28 promoted the immunogenicity of myeloma cells.

Human B7-1 gene was transducted into XG-s cells. CD28 agonist monoclonal antibody was primed. Primary allogeneic MLR, immunophenotypic analysis and quantitative measurement of IL-2 were performed.

XG cells were successfully transfected with B7-1 cDNA. The expressions of CD54, CD58, CD11a/CD18, CD40, CD40L, CD56, B7-2(CD86), HLA-I and HLA-II molecules were not affected by the transfection. The transduction of B7 gene dramatically increased the immunogenicity of tumor cells. In allo-MLR, the B7-1 expressing XG cell could more effectively mediate the activation, proliferation and IL-2 secretion of alloantigenic CD8+ T cells than XG cells did. Like B7-1 molecules, anti-CD28 agonistic McAb could induce the MLR of allo-T cell.

Human multiple myeloma cells failed to induce antitumor immunoreaction because of the weak expression of B7 molecules. The transfection of B7-1 or CD28 agonist antibody could stimulate and proliferate T lymphocytes and increase the immunogenicity of myeloma cells. CD28 agonist antibody might be promising for clinical application.