摘要
Introduction: Recent evidence suggests that agents which modulate the nature of the immune response may be effective in preventing or treating autoimmune disease. We recently reported that the non-toxic B-subunit of E. coli heat-labile enterotoxin (EtxB) exerts profound modulatory effects on lymphocyte populations in vitro; notably the polyclonal activation of B-cells, apoptosis in CD8+ T-cells and to have a negligible direct effect on CD4+ T-cells. The failure of a non-receptor binding mutant of EtxB, EtxB (G33D), to cause such effects provided unequivocal evidence for a critical role of receptor interaction in mediating these events. The receptor which EtxB binds to is a ubiquitous cell surface glycolipid, GM1 ganglioside.