The corneal allograft response is a typical DTH response [45-48], and resembles the allograft response in other organs. The integrity of the blood-eye barrier is breached, resulting in an influx of white cells and proteins into the anterior chamber and cornea. Fibrin accumulates in the anterior chamber and white cells can be seen circulating in the convection currents in the aqueous humor. The cornea becomes infiltrated with macrophages, monocytes, neu-trophils, CD4-positive and CD8-positive T cells [47, 49-52]. It is clear from experimental systems that CD4-positive cells have a crucial role in the corneal allograft response . Therapeutic strategies directed at this cell as a means of suppressing the corneal allograft response are attractive. Humoral responses do not seem to be important. Patients who have rejected corneal grafts do develop donor-specific antibodies [54, 55], but corneal grafts are rejected in antibody-deficient hosts . The allograft response can be directed at all of the cellular components of the eye, but it is damage to the corneal endothe-lium which is critical. This layer of cells has minimal replicative capacity . Unlike the other corneal cells of donor origin, endothelial cells persist in the graft but in decreased num
4.10 Current Approaches to Immunomodulation for Corneal Transplantation
bers and with a slow attrition rate. Because en-dothelium is the only persisting donor element in corneal grafts and because it has a vital function, keeping the cornea transparent, and little capacity for coping with damage, endothelial rejection is the most damaging aspect of the corneal allograft response.
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