| First Author | De Paiva CS | Year | 2009 |
| Journal | Mucosal Immunol | Volume | 2 |
| Issue | 3 | Pages | 243-53 |
| PubMed ID | 19242409 | Mgi Jnum | J:191918 |
| Mgi Id | MGI:5463556 | Doi | 10.1038/mi.2009.5 |
| Citation | De Paiva CS, et al. (2009) IL-17 disrupts corneal barrier following desiccating stress. Mucosal Immunol 2(3):243-53 |
| abstractText | T helper (Th)-17 is a recently identified subtype of Th response that has been implicated in host defense and autoimmunity. We investigated whether there is evidence for a Th-17 response in human and experimental murine dry eye (DE). Gene expression in the human DE conjunctiva showed increased levels of the Th-17 inducers, interleukin (IL)-23, IL-17A, and interferon-gamma (IFN-gamma). In the murine model, we found that desiccating stress increased matrix metalloproteinase-9, Th-17-associated genes (IL-6, IL-23, transforming growth factor-beta1 and -2, IL-23R, IL-17R, IL-17A, retinoid-related orphan receptor-gammat, and CC chemokine attractant ligand-20) and IFN-gamma in cornea and conjunctiva. Furthermore, we found a significantly increased concentration of IL-17 in tears and number of IL-17-producing cells on the ocular surface. Antibody neutralization of IL-17 ameliorated experimental DE-induced corneal epithelial barrier dysfunction and decreased the expression of matrix metalloproteinases 3 and 9. Taken together, these findings suggest that IL-17 has a role in corneal epithelial barrier disruption in DE. |
