The aim of the corneal transplant in man is to maintain corneal transparency. Even under the best conditions a proportion of the grafts that initially "take" suffer from the clinical problem of "graft sickness" with late clouding. These grafts are the homoplastic type, and evidence is accumulating which indicates that the homograft rejection phenomenon in the cornea is an immune response.1,2 Thus, the clouding in an otherwise successful graft would result from a reaction of the host to the antigen of the donor tissue.
An observation made by Merwin and Hill,3 in working with subcutaneous homografts in mice, was that only those grafts which did not vascularize survive. This led to further studies and observations that homografts in cell-impervious millipore membranes survived in normal and in tissue-immunized mice.4,5 From this and other experiments, it was concluded that in this example the antibodies cytotoxic to the homografts were
HANNA C, IRWIN ES. Fate of Cells in the Corneal Graft. Arch Ophthalmol. 1962;68(6):810–817. doi:10.1001/archopht.1962.00960030814016
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