Yamada J, Streilein J W
Schepens Eye Research Institute, Boston, MA 02114, USA.
Invest Ophthalmol Vis Sci. 1997 Dec;38(13):2833-43.
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.
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.
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.
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.
尽管长期接受原位角膜同种异体移植的小鼠表现出供体特异性前房相关免疫偏离（ACAID），但这种偏离反应直到移植命运确定很久之后才被检测到。为了确定角膜组织本身诱导ACAID的效率，将同种异体角膜片段插入正常小鼠眼的前房。
将C57BL/6（同种异体）和BALB/c（同基因）供体正常眼的中央角膜切成约0.3×2.0mm的楔形片段（在一些实验中去除角膜上皮），并插入受体内皮相邻的前房。评估这些片段受体的供体特异性迟发型超敏反应（DH）和ACAID，并测试含片段眼支持对无关抗原的ACAID的能力。
同基因和同种异体角膜在前房无限期存活，没有炎症或排斥的证据。虽然置于眼外部位的角膜片段（有或没有上皮层）是DH的有效诱导剂，但在眼内只有带上皮的移植物诱导DH。此外，这种DH反应是短暂的。前房内同种异体角膜片段的受体在8周时产生ACAID，但在1周时未产生。此外，当将牛血清白蛋白注入前房时，含片段眼支持ACAID诱导。
插入前房的同种异体角膜组织可诱导前房相关免疫偏离，但其发生延迟。这种延迟可能由移植物上供体上皮的持续存在决定，其促进DH。一旦上皮丢失，DH消失且ACAID出现。前房相关免疫偏离可能有助于维持角膜同种异体移植的存活。
