Expression of cell adhesion molecules in corneal graft failure

• Published in: Cornea Vol. 12; no. 6; p. 475
• Main Authors: Whitcup, S M, Nussenblatt, R B, Price, Jr, F W, Chan, C C
• Format: Journal Article
• Language: English
• Published: United States 01.11.1993
• Subjects: Antibodies, Monoclonal; Cell Adhesion; Cell Adhesion Molecules - metabolism; Cornea - metabolism; Cornea - surgery; Corneal Stroma - metabolism; E-Selectin; Endophthalmitis - complications; Endophthalmitis - metabolism; Graft Rejection - etiology; Graft Rejection - metabolism; Graft Rejection - surgery; HLA-DR Antigens - metabolism; Humans; Immunoenzyme Techniques; Intercellular Adhesion Molecule-1; Keratitis - metabolism; Keratoplasty, Penetrating; Reoperation; Vascular Cell Adhesion Molecule-1
• ISSN: 0277-3740
• DOI: 10.1097/00003226-199311000-00003

Corneal graft failure is frequently mediated by uncontrolled inflammatory disease. We studied the expression of cell adhesion molecules in seven penetrating keratoplasty specimens with graft failure and in a normal eye bank cornea using immunohistochemical staining and monoclonal antibodies against intercellular adhesion molecule-1 (ICAM-1, CD54), lymphocyte function-associated antigen-1 (LFA-1, CD11a/CD18), vascular cell adhesion molecule-1 (VCAM-1), E-selectin, and major histocompatibility complex (MHC) class II antigen (HLA-DR). ICAM-1 and HLA-DR were expressed on keratocytes and the corneal endothelium in six of the seven specimens. ICAM-1 expression was strongest in the corneas with the most severe inflammation (corneal allograft rejection and severe intraocular inflammation). LFA-1 is a counter-receptor for ICAM-1, and infiltration with leukocytes expressing either the alpha or beta chain of LFA-1 was found in areas of ICAM-1 expression in four of the seven corneas. In contrast, E-selectin was expressed in the stroma in only two specimens, and VCAM-1 in one specimen. Expression of cell adhesion molecules or MHC class II antigen were not detected in the normal eye bank cornea. These data suggest that ICAM-1 expression may play an important role in the development of corneal graft failure. Furthermore, monoclonal antibodies to block ICAM-1 or its ligands may inhibit the development of corneal inflammation.