Decay-accelerating factor expression may provide immunoprotection against antibody-mediated cardiac allograft rejection.

BACKGROUND: Not all patients with complement deposition of the heart have developed hemodynamic instability at the time of diagnosis, suggesting that immunoprotective mechanisms reside within grafts. We hypothesized that decay-accelerating factor (DAF) could provide a first-line defense against complement injury, thus explaining the discrepancy in hemodynamics. Thus, we examined the role of DAF in the clinical presentation of antibody-mediated cardiac allograft rejection.

METHODS: Endomyocardial biopsies from C4d(+)/C3d(+) patients were immunoflourescently stained for DAF, and its expression was compared in patients who did (n = 5) and did not (n = 4) exhibit allograft dysfunction.

RESULTS: Endomyocardial biopsies of patients without allograft dysfunction displayed intense staining of endothelial bound DAF expression at the time of antibody-mediated cardiac allograft rejection. Conversely, biopsies of patients with allograft dysfunction showed no evidence of DAF at that time.

CONCLUSIONS: Expression of DAF on cardiac allografts may provide an immunoprotective mechanism against the deleterious effects of complement deposition in patients with antibody-mediated cardiac allograft rejection.