title: Induction of anterior chamber-associated immune deviation by corneal allografts placed in the anterior chamber.
abstract: OBJECTIVE
  Although mice with long-accepted orthotopic corneal allografts display donor-specific anterior chamber-associated immune deviation (ACAID), this deviant response is not detected until well after the fate of the grafts is decided. To determine the efficiency with which corneal tissue itself can induce ACAID, allogeneic corneal segments were inserted into anterior chambers (AC) of normal mouse eyes.
  
  
  METHODS
  Central corneas from normal eyes of C57BL/6 (allogeneic) and BALB/c (syngeneic) donors were cut into wedge-shaped fragments measuring approximately 0.3 x 2.0 mm (in some experiments the corneal epithelium was removed) and inserted into the AC adjacent to recipient endothelium. Recipients of these fragments were evaluated for donor-specific delayed hypersensitivity (DH) and ACAID, and fragment-containing eyes were tested for their capacity to support ACAID to an irrelevant antigen.
  
  
  RESULTS
  Syngeneic and allogeneic corneas survived indefinitely in the AC without evidence of inflammation or rejection. Although fragments of cornea (with or without epithelial layers) placed at extraocular sites were potent inducers of DH, within the eye only epithelium-bearing grafts induced DH. Moreover, this DH response was short-lived. Recipients of allogeneic corneal fragments in the AC developed ACAID by 8 weeks, but not at 1 week. Moreover, fragment-containing eyes supported ACAID induction when bovine serum albumin was injected into the AC.
  
  
  CONCLUSIONS
  Anterior chamber-associated immune deviation can be induced by allogeneic corneal tissue inserted into the AC, but its onset is delayed. The delay may be dictated by persistence of donor epithelium on the graft, which promotes DH. Once the epithelium is lost, DH disappears and ACAID emerges. Anterior chamber-associated immune deviation may contribute to the maintenance of corneal allograft viability.
authors.affiliation: Schepens Eye Research Institute, Boston, MA 02114, USA.
authors.forename: J
authors.initials: J
authors.lastname: Yamada
authors.forename: J W
authors.initials: JW
authors.lastname: Streilein
mesh_terms: D000818:Animals; D000867:Anterior Chamber / Q000276:immunology* / Q000601:surgery; D003315:Cornea / Q000276:immunology; D016039:Corneal Transplantation / Q000276:immunology*; D019573:Epithelium, Corneal / Q000276:immunology; D006085:Graft Survival / Q000276:immunology; D006968:Hypersensitivity, Delayed / Q000276:immunology*; D007249:Inflammation / Q000276:immunology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D012710:Serum Albumin, Bovine / Q000276:immunology; D014184:Transplantation, Homologous
chemical_list: D012710:Serum Albumin, Bovine