Aqueous Tear Deficiency Increases Conjunctival Interferon-γ (IFN-γ) Expression and Goblet Cell Loss

The number of mucin-filled conjunctival goblet cells (GC) has been found to decrease in aqueous-deficient dry eye and certain ocular surface inflammatory conditions, such as Stevens-Johnson syndrome and graft-versus-host disease (GVHD).1–4 The cause for GC loss in these dry eye/ocular surface diseases has not been established, but mouse models suggest it may be due to imbalanced expression of T helper (Th) cytokines, with increased levels of the Th1 cytokine interferon-γ (IFN-γ) and increased ratio of IFN-γ to the Th2 cytokine IL-13 (IFN-γ/IL-13).5,6 Altered ratios of these Th cytokines have been associated with hyperplasia or loss of GC in the airway and gut mucosa.7,8 Interleukin-13 has been found to promote GC differentiation in the conjunctival and airway epithelium, while IFN-γ has caused conjunctival GC loss in mice.6,7,9 Expression of these Th cytokines and their receptors in the conjunctiva and the relationship between levels of these cytokines and goblet cell density (GCD) and expression of cornified envelope precursors have not been studied in patients with tear dysfunction. The purpose of this study was to investigate the hypothesis that increased IFN-γ expression is associated with conjunctival GC loss and mucin deficiency in subjects with tear dysfunction.