The conjunctival mucosa has several similarities to the mucosal immune system of the gut and bronchus. Like the gut and bronchial mucosa, the conjunctiva is capable of inducing tolerance to encountered antigens and possesses a repertoire of CD8+ intraepithelial lymphocytes (IELs) bearing the human mucosal lymphocyte-1 antigen (HML-1) which has been shown to be an alpha E beta 7 integrin. The epithelial cells surface ligand for HML-1 is E-cadherin. The distribution of E-cadherin in the normal human conjunctiva and cornea is not known. We investigated E-cadherin distribution in the conjunctiva and cornea by immunohistochemistry. E-cadherin was found to be present in all layers of the conjunctival epithelium but not in corneal epithelium. In the conjunctiva it may act as a ligand for the HML-1+ IELs. The specific location of IELs along the basal cells of the conjunctiva compared with the generalised distribution of E-cadherin through all layers, indicates that factors other than E-cadherin binding determine the distribution of HML-1+ IELs. We performed electron microscopy on de-epithelialised conjunctival and corneal samples. We demonstrated the presence of epithelial basement membrane pores in the conjunctiva but not in the cornea. Lymphocyte migration from the substantia propria to the intraepithelial compartment appears to occur through these pores, which may also serve as a conduit for antigen presentation by epithelial antigen presenting cells (APCs) to lymphocytes in the substantia propria.

Cell-matrix interactions play a fundamental role in normal and pathological conditions. They can be mediated by the cytoadhesin subgroup of the integrin superfamily of adhesion molecules. Its members include the vitronectin receptor (VNR) and the platelet glycoprotein IIb/IIIa (GP IIb/IIIa). Both receptors are composed of an alpha-chain (alpha v and alpha IIb, respectively) coupled to a beta 3-chain. Using in situ immunohistochemistry and monoclonal antibodies, the authors studied the distribution of GP IIIa (common beta 3-chain), GP IIb/IIIa (alpha IIb-chain) and VNR (alpha v-chain) in normal and pathological corneal tissues. In the normal cornea, the limbal vascular endothelium was weakly alpha v-positive. Occasionally, faint and granular staining was seen in the epithelium. In the pathological samples, an upregulated expression of the alpha v-chain was noticed on the corneal epithelium as well as on fibroblasts and corneal endothelium. The alpha IIb and beta 3-chains were consistently absent. These data suggest that expression of the VNR-alpha v-chain in the human cornea is modulated by soluble factors released during inflammation and wound healing. Dissociation of expression of the alpha v and beta 3-chains suggests usage of an alternative beta-chain by the VNR-alpha v-chain.

No abstract