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• W2046130726 abstract "To the editor: The article “IL-17 disrupts corneal barrier following desiccating stress” by De Paiva et al.1De Paiva CS IL-17 disrupts corneal barrier following desiccating stress.Mucosal Immunol. 2009; 2,: 243-25310.1038/mi.2009.5Abstract Full Text Full Text PDF PubMed Scopus (303) Google Scholar provides additional evidence that interleukin-17 (IL-17) is associated with disruption of the corneal epithelial barrier function, which is the most sight-threatening complication of dry eye disease (DE), arguably the most common ophthalmologic condition. It reports an increased expression of Th17-cell inducers, including IL-6, transforming growth factor-β, IL-23, and IL-17A on the ocular surface of DE patients, as well as an increased concentration of IL-17 in tears and an increased number of Th17 cells on the ocular surface of experimental animals with DE. In addition, the authors show that IL-17-induced secretion of MMP-3 and -9 by epithelial cells causes a significant increase in corneal epithelial permeability, which is ameliorated by in-vivo neutralization of IL-17. However, the precise etiopathogenesis of DE, particularly the nature of ocular surface autoantigen(s), and the site and mechanism of generation of these self-reactive T cells are still not very clear.2Pflugfelder SC de Paiva CS Li DQ Stern ME Epithelial-immune cell interaction in dry eye.Cornea. 2008; 27: S9-S1110.1097/ICO.0b013e31817f4075Crossref PubMed Scopus (87) Google Scholar, 3Research in dry eye: report of the Research Subcommittee of the International Dry Eye WorkShop. Ocul. Surf. 5,, 179–193 (2007).Google Scholar, 4Barabino S Dana MR Dry eye syndromes.Chem. Immunol. Allergy. 2007; 92,: 176-18410.1159/000099268Crossref PubMed Scopus (45) Google Scholar In a recent article,5Chauhan SK Autoimmunity in dry eye is due to resistance of Th17 to Treg suppression.J. Immunol. 2009; 182,: 1247-125210.4049/jimmunol.182.3.1247Crossref PubMed Scopus (227) Google Scholar we have shown not only the involvement of Th17 cells in dry eye pathogenesis but also the mechanism of induction of autoimmunity in the draining lymph nodes (LN) using a mouse model of DE. In addition to the expression of Th17 profile on the ocular surface, we showed increased frequency of Th17 cells in the draining LN, where these cells show specific resistance to regulatory T cell (Treg)-mediated suppression. In agreement with De Pavia et al.,1De Paiva CS IL-17 disrupts corneal barrier following desiccating stress.Mucosal Immunol. 2009; 2,: 243-25310.1038/mi.2009.5Abstract Full Text Full Text PDF PubMed Scopus (303) Google Scholar the functional relevance of Th17 cells in the pathogenesis of DE was fundamentally confirmed by an observation that the in-vivo neutralization of IL-17 results in a markedly attenuated induction and severity of disease. Interestingly, DE amelioration was paralleled by a reduction in the expansion of Th17 cells and by the prevention of the loss of Treg function in the draining LN, suggesting that the Th17 cell-secreted IL-17 antagonizes the Treg function, which in turn unleashes Th17 and Th1 cells to expand further, migrate to ocular surface, and cause epithelial damage. Together, these studies suggest that Th17 cells are the dominant pathogenic effectors in DE. On the basis of the current data1De Paiva CS IL-17 disrupts corneal barrier following desiccating stress.Mucosal Immunol. 2009; 2,: 243-25310.1038/mi.2009.5Abstract Full Text Full Text PDF PubMed Scopus (303) Google Scholar, 5Chauhan SK Autoimmunity in dry eye is due to resistance of Th17 to Treg suppression.J. Immunol. 2009; 182,: 1247-125210.4049/jimmunol.182.3.1247Crossref PubMed Scopus (227) Google Scholar and data published earlier2Pflugfelder SC de Paiva CS Li DQ Stern ME Epithelial-immune cell interaction in dry eye.Cornea. 2008; 27: S9-S1110.1097/ICO.0b013e31817f4075Crossref PubMed Scopus (87) Google Scholar, 3Research in dry eye: report of the Research Subcommittee of the International Dry Eye WorkShop. Ocul. Surf. 5,, 179–193 (2007).Google Scholar, 4Barabino S Dana MR Dry eye syndromes.Chem. Immunol. Allergy. 2007; 92,: 176-18410.1159/000099268Crossref PubMed Scopus (45) Google Scholar, an overarching hypothesis about the mechanism(s) involved in the pathogenesis of DE is illustrated in Figure 1. DE affects the visual performance and the quality of life of>10 million people in the United States alone. The current finding that IL-17 blockade leads to diminished disease severity suggests potential new approaches for the treatment of DE. The authors declared no conflict of interest. This work was supported in part by National Institutes of Health grant NEI R01-12963. Download .ppt (.43 MB) Help with ppt files PowerPoint slide for Fig. 1" @default.
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• W2046130726 title "Role of Th17 cells in the immunopathogenesis of dry eye disease" @default.
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• W2046130726 doi "https://doi.org/10.1038/mi.2009.21" @default.
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