Alain Goguel

Correlation between tear IgE levels and HLA-DR expression by conjunctival cells in allergic and nonallergic chronic conjunctivitis

Abstract Background: Chronic conjunctival inflammatory diseases may depend upon various mechanisms. Discriminating allergy from nonspecific inflammation has become of striking importance for diagnosis and treatment. We investigated conjunctival inflammatory response by comparing two objective biological tools, tear IgE and HLA-DR expression by conjunctival epithelium, as indirect indicators of activation of the Th2 and Th1 subsets, respectiv-ely. Methods: Eighty-two patients with chronic conjunctivitis underwent tear IgE measurement by an ELISA technique and quantitation of HLA-DR expression in impression cytology specimens. Forty-two had direct or indirect clinical indications of allergic mechanisms, 26 had chronic conjunctivitis without any sign of allergy, and 14 suffered from isolated nonallergic dry eyes. Results: Patients clinically considered as allergic only showed positive IgE in 47 of 84 eyes (56%), whereas 21% and 25% of eyes with nonspecific conjunctivitis and dry eyes respectively were also positive. IgE levels were significantly higher in the allergic group than in the other two groups. HLA-DR positivity in epithelial cells was found in 28.5%, 48% and 50% of eyes, respectively. HLA-DR expression by epithelial cells was negatively correlated with tear IgE, as most specimens positive to one criterion were negative to the other one (49 eyes DR+, IgE–; 47 eyes DR–, IgE+; only 9 eyes positive to both criteria; chi-square: P=0.0001). Conclusion: As IgE synthesis and HLA-DR induction may represent indirect indicators of the activation of the Th2 and Th1 subsets, association of these two simple tests could be interesting for the routine assessment of the mechanisms of inflammatory ocular surface diseases.

Flow cytometric analysis of the inflammatory marker HLA DR in dry eye syndrome: results from 12 months of randomized treatment with topical cyclosporin A.

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 Sjogren’ 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.