RESEARCH - Autoimmunity in dry eye is due to resistance of Th17 to Treg suppression

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J Immunol. 2009 Feb 1;182(3):1247-52.

Autoimmunity in dry eye is due to resistance of Th17 to Treg suppression.

Chauhan SK, El n J, Ecoiffier T, Goyal S, Zhang Q, Saban DR, Dana R.

Schepens Eye Research Institute, Harvard Medical School, Boston, MA 02114, USA.

Dry eye disease (DED), an inflammatory autoimmune disorder affecting

the ocular surface, degrades visual performance and the quality of

life of >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 that is associated specifically

with Treg dysfunction and disease pathogenesis and suggest a new

target for dry eye therapy.

PMID: 19155469

http://www.ncbi.nlm.nih.gov/pubmed/19155469

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