IL17A and cystic fibrosis: The absence of detectable coexisting infection suggests that this may be a potential mechanism for chronic neutrophil elevation or an undetectable alteration in the diseased ocular microbiome driving the immune response.45 In a fungal model of keratitis, neutrophils demonstrate increased elastase and MMP-9 activity via autocrine production of IL-17 in response to IL-6 and IL-23.46,47 In addition, in cystic fibrosis, pseudomonal infection induces a persistent elevated inflammatory response to IL-17.