Biol. Pharm. Bull. 30(4) 655—660 (2007)

netically controlled mechanism by which multicellular organisms to regulate normal cell development, tissue homeostasis, and immunological responses. During apoptosis, various cellular events occur, including morphological changes, exposure of phosphatidylserine (PS) on the cell surface, and fragmentation of nuclei. Molecules on the surfaces of apoptotic cells are recognized by macrophages and neighboring resident cells, which then ingest the apoptotic cells via phagocytosis. Cytotoxic T lymphocytes (CTLs) and natural killer (NK) cells play key roles in the immune response to virus-infected and malignant cells. CTLs and NK cells induce target cell apoptosis through one of two mechanisms: interaction between Fas ligand on the CTL or NK surface and its receptor on the target cell and release of cytotoxic granules containing perforin, a pore-forming protein, and granzymes, a family of serine proteases. Within the granzyme family, granzyme B is the most powerful proapoptotic protease. Granzyme B can induce target cell apoptosis by cleaving a variety of intracellular proteins, such as procaspase 3, procaspase 8, mitochondrial Bid, and poly (ADP-ribose) polymerase. Perforin or granzyme B alone are not sufficient to induce apoptosis of target cells, and the two appear to work in concert. Specifically, granzyme B must be incorporated into the target cells, and this is mediated by coreleased perforin or by receptors on the target cell. In in vitro studies, granzyme B has been incorporated into target cells using perforin purified from CTLs or NK cells, adenovirus, or BioPORTER, a cationic lipid formulation. In a previous report, we showed that during apoptosis in Jurkat cells, a human acute lymphoblastoma cell line, the cell surface expression of the Lewis X and Y antigens (Galb14(Fuca1-3)GlcNAc and Fuca1-2Galb1-4(Fuca1-3)GlcNAc, respectively) and the expression of mRNA encoding a1,3-fucosyltransferase (FUT) 4 were up-regulated downstream of caspase 3 activation. In the present study, we induced apoptosis in Jurkat cells by incorporation of granzyme B using BioPORTER, and we measured the cell surface expression of Lewis X and Y antigens and the roles of caspases in their cell surface expression.