Flow Cytometric Analysis of the Inflammatory Marker HLA DR in Dry Eye Syndrome: Results from 12 Months of Randomized Treatment with Topical Cyclosporin A

Abstract

Dry eye disease or keratoconjunctivitis sicca (KCS) is a common ocular surface disease that causes chronic ocular irritation and dry or gritty sensations of the ocular surface. Traditionally, KCS has been described as a secretion disorder of the lacrimal glands that leads to a deficiency in tear production. However, a growing body of evidence suggests KCS has a complex multifactorial etiology, which comprises tear dysfunction and a localized immune-mediated inflammatory response affecting the entire ocular surface (Stern et al., 1998). The inflammatory response observed in KCS patients with and without Sjögren’ s syndrome (SS) encompasses cellular and immunopathological abnormalities of the conjunctival epithelium including upregulation of inflammatory cytokines and molecular markers of the inflammatory pathway (Baudouin et al., 1992;Jones et al., 1994; Pflugfelder et al 1990;1999;Tsubota et al., 1999a;Smith et al., 2000). Mircheff and colleagues (1994) proposed that in KCS patients without SS, this inflammatory process results from altered membrane “trafficking” of the lacrimal acinar cells. These authors suggested that these changes arise due to expression of major histocompatibility (1999). Furthermore, epithelial cells produce TNF-a (Jones et al., 1998). Consequently, it can be postulated that this combination of increased HLA DR antigen expression and elevated levels of inflammatory cytokines within the conjunctival epithelium may represent the focus for cytotoxic reactions between epithelial cells and infiltrating lymphocytes, which would also help to perpetuate the local immune response.