Ocular allergic disease

Purpose of review This review will focus on recent advances in our understanding of the pathogenesis of allergic eye diseases. Common findings in acute allergic conjunctivitis (seasonal and perennial) and chronic allergic conjunctivitis (vernal keratoconjunctivitis, atopic keratoconjunctivitis, and giant papillary conjunctivitis) include evidence of mast cell activation and eosinophil attraction and activation. Cytokine levels found in tears, conjunctival impression cytology and biopsy specimens, and serum have been evaluated as markers of disease, and as targets of therapeutic intervention. Recent findings Human conjunctival epithelial cells respond to tumor necrosis factor alpha, interleukin-1 beta, and interferon-gamma individually and in combination. Intracellular adhesion molecule-1 expression is upregulated by interleukin-1 beta and tumor necrosis factor a. Conjunctival epithelial cells release interleukin-8 in response to interleukin-1 beta and tumor necrosis factor alpha but not interferon-gamma. Supernatants from activated mast cells cause increased adhesion of eosinophils to conjunctival epithelium. Tear levels of tumor necrosis factor a were elevated in vernal keratoconjunctivitis patients compared with normal controls. T cell lines from chronic allergic eye disease patients showed inconsistent production of cytokines in atopic and vernal keratoconjunctivitis and low levels in giant papillary conjunctivitis. Vernal keratoconjunctivitis patients have differing levels of eosinophil cationic protein in their serum if they were serum specific immunoglobulin E positive compared to serum specific immunoglobulin E negative patients. Summary Recent findings continue to expand our basic knowledge of mechanisms and differences between seasonal and perennial allergic conjunctivitis and atopic and vernal keratoconjunctivitis. Understanding the complex interactions and cross talk between cells, cytokines and other mediators is relevant for new therapeutic approaches directed at specific disease entities.