The Journal of Experimental Medicine
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Published online October 29, 2007
doi:10.1084/jem.20070994
The Journal of Experimental Medicine, Vol. 204, No. 12, 2825-2835
The Rockefeller University Press, 0022-1007 $30.00
© 2007 Moisan et al.
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ARTICLE

 Ets-1 is a negative regulator of Th17 differentiation

Jacques Moisan1, Roland Grenningloh1, Estelle Bettelli2, Mohamed Oukka2, and I-Cheng Ho1

1 Rheumatology, Immunology and Allergy, 2 Center for Neurologic Disease, Brigham and Women's Hospital/Harvard Medical School, Boston, MA 02115

CORRESPONDENCE I-Cheng Ho: iho{at}partners.org

IL-17 is a proinflammatory cytokine that plays a role in the clearance of extracellular bacteria and contributes to the pathology of many autoimmune and allergic conditions. IL-17 is produced mainly by a newly characterized subset of T helper (Th) cells termed Th17. Although the role of Th17 cells in the pathology of autoimmune diseases is well established, the transcription factors regulating the differentiation of Th17 cells remain poorly characterized. We report that Ets-1–deficient Th cells differentiated more efficiently to Th17 cells than wild-type cells. This was attributed to both low IL-2 production and increased resistance to the inhibitory effect of IL-2 on Th17 differentiation. The resistance to IL-2 suppression was caused by a defect downstream of STAT5 phosphorylation, but was not caused by a difference in the level of ROR{gamma}t. Furthermore, Ets-1–deficient mice contained an abnormally high level of IL-17 transcripts in their lungs and exhibited increased mucus production by airway epithelial cells in an IL-17–dependent manner. Based on these observations, we report that Ets-1 is a negative regulator of Th17 differentiation.

Abbreviations used: CHIP, chromatin immunoprecipitation; ICS, intracellular cytokine staining; PAS, periodic acid Schiff.


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