Purpose: The expression of cellular adhesion molecules in 31 penetrati
ng keratoplasty specimens from a broad range of corneal inflammatory d
iseases was studied using monoclonal antibodies and an immunoperoxidas
e technique. Methods: Corneas were divided into noninflamed, mild to m
oderately inflamed, and severely inflamed groups based on histologic f
indings. The panel of adhesion molecules studied included HLA-ABC, HLA
-DR, CD3, LFA-1, MAC-1, ICAM-1, PECAM-1, VCAM-1, and E-selectin-1. Res
ults: The adhesion molecules ICAM-1, HLA-DR, PECAM-1, CD3, VCAM-1, LFA
-1, and MAC-1 were selectively expressed in areas of corneal inflammat
ion. In general, HLA-DR and intercellular adhesion molecule ICAM-1 wer
e co-expressed in similar regions. PECAM-1 was restricted to zones of
marked inflammation and vascularization. E-selectin-1 was detected onl
y in the stroma of a graft melt in a patient with active ocular cicatr
icial pemphigoid, and may reflect a primary regulatory dysfunction in
this disorder. The ICAM-1 ligand was, in general, more diffusely distr
ibuted than its receptor LFA-1, a beta-2 integrin found on leukocyte c
ell membranes. The localization of the integrin MAC-1, present on macr
ophages, neutrophils, and some lymphocytes, did not always parallel th
e staining pattern of ICAM-1, suggesting promiscuity in its binding to
other ligands besides ICAM-1. Conclusions: Adhesion molecules are det
ected readily at sites of corneal inflammation and may play a critical
role in facilitating the recruitment of immune regulatory cells to th
ese areas. Future efforts to block or modulate the expression of inter
cellular adhesion molecules may provide new therapeutic options in the
treatment of corneal inflammatory diseases.