Intragraft immune events causing vascularized organ graft rejection
These studies indicate that CTLs are only one component of inexorable vascularized organ graft rejection. Although these cells are undeniably cytodestructive in vivo, abrogation of humoral injury by enhancing antibody allows graft recovery and longterm function. The remarkable absence of anti-Ia-like antibodies in the enhanced host suggests that anti-Ia responses contribute substantially to allograft rejection. Perhaps this response is abolished by suppressor cells in the enhanced recipient. It is likely that the entire repetoire of potentieal immunologic assault mechanisms are unleashed during unmodified rejection, including activation of both cellular and humoral effector arcs directed against both classical an nonclassical (Ia-like)MHC incompatibilities and other minor transplant antigens. We consider it unlikely that the rejection of vascularized organ grafts is the sole and specialized province of CTLs or even cell-mediated immunity. Graft death appears to result from a composite of cellular and humoral mechanisms.