Together, these data suggest that the overexpression in scarring trachoma of CCL20, IL23A, IL19, IL1B, and S100A7 could reflect mechanisms of pathogenesis similar to those observed in psoriasis and intestinal inflammation, whereby the upregulation of IL23A and IL1B promotes the recruitment and activity of pathogenic IL-23A-responsive cells (Th17, ILC, or γδ T cells, for example), which drive proinflammatory responses in the conjunctival epithelium, leading to chronic inflammation and fibrosis. The gene discussed is S100A7; the disease is inclusion conjunctivitis.