INDUCTION OF HIGH-AFFINITY FIBROBLAST GROWTH-FACTOR RECEPTOR EXPRESSION AND PROLIFERATION IN HUMAN ENDOTHELIAL-CELLS BY ANTI-HLA ANTIBODIES- A POSSIBLE MECHANISM FOR TRANSPLANT ATHEROSCLEROSIS
Pe. Harris et al., INDUCTION OF HIGH-AFFINITY FIBROBLAST GROWTH-FACTOR RECEPTOR EXPRESSION AND PROLIFERATION IN HUMAN ENDOTHELIAL-CELLS BY ANTI-HLA ANTIBODIES- A POSSIBLE MECHANISM FOR TRANSPLANT ATHEROSCLEROSIS, The Journal of immunology, 159(11), 1997, pp. 5697-5704
The major limitation to long term survival of organ allografts is chro
nic rejection, which is manifested as atherosclerosis of the vessels o
f the transplanted organ, There is a significant association between t
ransplant atherosclerosis and the development of Abs to the disparate
HLA Ags present on the graft vasculature, We have investigated the eff
ect of anti-HLA Abs on endothelial cells (EC) and smooth muscle cells
cultured in vitro. Ab ligation of class I molecules on ECs results in
increased high affinity fibroblast growth factor receptor mRNA express
ion, and enhanced basic fibroblast growth factor ligand binding. Ab bi
nding to class I molecules on EC and smooth muscle cells is also accom
panied by augmented cell proliferation, These results suggest that the
intimal thickening observed in transplant atherosclerosis is the resu
lt of the proliferative effects of anti-HLA Abs.