Showing papers by "Huan Guo published in 2001"

A study of human DAF, cd59, MCP transgene in xenotransplantation☆

Abstract: USE of animal organ has been accepted as a realistic option to overcome the shortage of organ donors for transplantation. Complement activation plays a pivotal role in hyperacute xenograft rejection. Under physiological conditions, activation of complement on endothelial cells is partly regulated by complement regulatory proteins (CRPs) such as DAF (CD55), MCP (CD46), and CD59. Both DAF and CD46 act at the level of C3/C5 convertases, whereas CD59 binds to C9 of the C5b–9 complex, preventing the formation of the membrane-attack complex. Because complement activation is caused by an inability of CRPs to regulate complement cascade across species, the susceptibility of a xenograft to complement mediated injury may therefore be due to the failure of donor CRPs to regulate activation of recipient complement. Our experimental approach to prevent the complement-mediated hyperacute xenograft rejection has been suggested to generate transgenic mice and pigs, which express human decay accelerating factor (hDAF). Moreover, hDAF and MCP or DAF and CD59-double transgenic porcine endothelial cells are more protected from human complement attack.