Ld. Devitohaynes et al., DONOR-DERIVED HUMAN-LEUKOCYTE ANTIGEN CLASS-I PROTEINS IN THE SERUM OF HEART-TRANSPLANT RECIPIENTS, The Journal of heart and lung transplantation, 15(10), 1996, pp. 1012-1026
Background: Human leukocyte antigen class I proteins are expressed on
most cell types in all organ allografts but are constituitively secret
ed only by certain organs, for example, the liver. We hypothesized tha
t detectable levels of donor-derived human leukocyte antigen proteins
would be released from transplanted cardiac allografts only when the a
llograft was immunologically stimulated, that is, during rejection and
perhaps during viral infection. If so, then the release of donor huma
n leukocyte antigen might be a noninvasive monitor of these events. Me
thods: We used an enzyme-linked immunosorbent assay to detect donor-de
rived human leukocyte antigen-A2 in the serum of 21 human leukocyte an
tigen-A2 negative recipients of human leukocyte antigen-A2-positive he
art transplants. The level of donor human leukocyte antigen-A2 during
the first 100 days after transplantation was correlated with the clini
cal status of the patient. Results: We found little or no donor human
leukocyte antigen in the serum of heart transplant recipients whose po
stoperative clinical course was unremarkable for infection or rejectio
n. We did find donor-derived human leukocyte antigen in the serum of h
eart transplant recipients transiently in the week immediately after t
ransplantation, continuously from patients in whom chronic rejection w
as developing, during cytomegalovirus infection, and during some, but
not all, acute rejection episodes as determined by endomyocardial biop
sy. Conclusions: These findings are consistent with the hypothesis tha
t the donor human leukocyte antigen serum level reflects vascular dise
ases, rather than myocardial disease in the transplanted heart. Theref
ore, the serum level of donor human leukocyte antigen cannot be used a
s a monitor of cellular infiltration and myocyte damage as currently a
ssessed by endomyocardial biopsy but may be an early indicator of the
development of vascular disease such as chronic rejection.