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Cornea. 1993 Nov;12(6):475-80.

Expression of cell adhesion molecules in corneal graft failure.

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Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, Maryland 20892.


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.

[Indexed for MEDLINE]

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