Anterior Chamber-Associated Immune Deviation (ACAID) promotes corneal allograft survival

Purpose. To investigate the role of anterior chamber-associated immune deviation (ACAID) in promoting corneal allograft survival. Methods. CB6F1 mice (H-2^b/d) were primed in the anterior chamber (AC) with either corneal epithelial and endothelial cells or spleen cells from either C3H or NZB donors 7 days prior to receiving corneal transplants from either fully allogeneic (MHC + multiple minor disparities; C3H) or multiple minor H disparate (NZB) donors. Results. AC priming with donor-specific spleen cells resulted in doubling of the mean survival time (MST) in recipients of fully allogeneic C3H corneal grafts (MST=37 days) compared to untreated controls (HST = 18 days). Similar experiments using Langerhans cell-containing (LC⁺), multiple minor H disparate NZB corneal grafts indicated that AC priming with NZB spleen cells produced a sharp reduction in the incidence of graft rejection (35% rejection) compared to untreated controls (80% rejection) or mice primed in the AC with corneal cells (100% rejection). Since an intact spleen is necessary for the induction and maintenance of ACAID, unprimed CB6F1 mice were splenectomized and challenged with orthotopic NZB corneal allografts. As in previous experiments, only 29% of the Langerhans cell free (LC^-) NZB corneal grafts were rejected in unprimed CB6F1 hosts. By contrast, 91% of LC^- NZB grafts were rejected in splenectomized CB6F1 hosts. Conclusions. Corneal graft survival can be enhanced through the induction of ACAID while maneuvers that abrogate ACAID (e.g., splenectomy) promote corneal allograft rejection.