The Journal of Immunology · 1992 · 124 citations · 0 references
Life SciencesImmunologyAdaptive ImmunityCancer ImmunologyImmunoregulationLymphocyte ActivationT Cell ActivationT Cell BiologyT Cell Receptor SignalingB7 Family Immunoregulatory LigandsCd28 CostimulationCd28 SignalingCostimulatory Signal ModulationCostimulatory Signal TransductionMhc Class Ii Molecules
Previous studies demonstrated that a human pre-B acute lymphoblastic leukemia cell line, NALM-6, failed to stimulate a primary MLR, despite expression of class II MHC and adhesion molecules. Here we demonstrate that this is the result of the fact that NALM-6 cells do not express the ligand for CD28, namely B7. NALM-6 transfectants that expressed high levels of B7 gained the capacity to stimulate IL-2 production by class II MHC molecule-specific alloreactive T cells and to costimulate a polyclonal population of purified T cells cultured with immobilized anti-CD3 mAb. In the presence of PMA, NALM-6 cells transfected with B7 polyclonally stimulated T cells in a cyclosporine A-resistant fashion, a property previously attributed only to agonistic anti-CD28 mAb. The gain of these functions could not be explained solely by an increased capacity of the transfectants to form conjugates with T cells, suggesting that the CD28/B7 interaction transduces a costimulatory signal in T cells.