IL-17 disrupts corneal barrier following desiccating stress

C. S. De Paiva, S. Chotikavanich, S. B. Pangelinan, J. D. Pitcher, B. Fang, X. Zheng, P. Ma, W. J. Farley, K. F. Siemasko, J. Y. Niederkorn, M. E. Stern, D. Q. Li, S. C. Pflugfelder

Research output: Contribution to journalArticlepeer-review

321 Scopus citations


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-γ). In the murine model, we found that desiccating stress increased matrix metalloproteinase-9, Th-17-associated genes (IL-6, IL-23, transforming growth factor-β1 and -2, IL-23R, IL-17R, IL-17A, retinoid-related orphan receptor-γt, and CC chemokine attractant ligand-20) and IFN-γ 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.

Original languageEnglish (US)
Pages (from-to)243-253
Number of pages11
JournalMucosal Immunology
Issue number3
StatePublished - 2009

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology


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