Corneal allograft rejection.

The cornea is avascular, enjoys relative immune privilege, and immunosuppressive treatment can be directly applied: yet data from all available reports indicate that allogeneic rejection is the commonest cause of corneal graft failure. In Australia, 5 year actuarial corneal graft survival is 72%: irreversible rejection accounts for at least 33% of all graft failures.' Graft survival is much shorter in certain high risk groups, with rejection being the primary cause of failure in a higher proportion."4 Moreover, graft survival figures give no indication of the number of patients denied the opportunity of a graft in the first place because of perceived high risk of rejection, and in corneal surgery at the present time the main strategy to reduce the impact of graft rejection is to avoid grafts in high risk cases. The fact that rejection can be diagnosed, and its clinical course studied, by direct observation of corneal grafts obviates the need for histopathological study of biopsy specimens of graft. Biopsy of rejecting cornea could not be justified ethically. This constraint does not apply to human solid organ transplants: investigation of immunohistochemical, ultrastructural, and molecular aspects of rejection of kidney and other organs is well established and can guide clinical management. The virtual inaccessibility of rejecting human cornea from the biopsy standpoint, and the fact that grafts are seldom removed at the time of rejection, has two consequences for the investigation of mechanisms of graft rejection. Firstly, the corneal grafts on which pathological studies have been reported represent late or burnt out rejection. Secondly, most information on the sequence of events in rejecting corneas has been obtained from experimental animal models. Thus, while corneal graft rejection presents clinical appearances familiar to ophthalmologists, our knowledge of pathology and mechanisms is comparatively fragmentary.