Autoimmunity in Dry Eye Is Due to Resistance of Th17 to Treg Suppression
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Author
El Annan, Jaafar
Ecoiffier, Tatiana
Goyal, Sunali
Zhang, Q.
Saban, Daniel R.
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https://doi.org/10.4049/jimmunol.182.3.1247Metadata
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Chauhan, S. K., J. El Annan, T. Ecoiffier, S. Goyal, Q. Zhang, D. R. Saban, and R. Dana. 2009. “Autoimmunity in Dry Eye Is Due to Resistance of Th17 to Treg Suppression.” The Journal of Immunology 182 (3) (January 20): 1247–1252. doi:10.4049/jimmunol.182.3.1247.Abstract
Dry eye disease (DED), an inflammatory autoimmune disorder affecting the ocular surface, degrades visual performance and the quality of life of more than 10 million people in the United States alone. The primary limitation in the effective treatment of DED is an incomplete understanding of its specific cellular and molecular pathogenic elements. Using a validated mouse model of DED, herein we functionally characterize the different T cell subsets, including regulatory T cells (Tregs) and pathogenic effector T cells, and determine their contribution to the pathogenesis of DED. Our data demonstrate the presence of dysfunctional Tregs and the resistance of pathogenic T cells, particularly Th17 cells, to Treg suppression in DED. In addition, we clearly show that in vivo blockade of IL-17 significantly reduces the severity and progression of disease, which is paralleled by a reduction in the expansion of Th17 cells and restoration of Treg function. Our findings elucidate involvement of a previously unknown pathogenic T cell subset (Th17) in DED which is associated specifically with Treg dysfunction and disease pathogenesis, and suggest a new target for dry eye therapy.Other Sources
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2630586/Terms of Use
This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAACitable link to this page
http://nrs.harvard.edu/urn-3:HUL.InstRepos:34622443
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