Journal
CELL
Volume 126, Issue 6, Pages 1121-1133Publisher
CELL PRESS
DOI: 10.1016/j.cell.2006.07.035
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IL-17-producing T lymphocytes have been recently shown to comprise a distinct lineage of proinflammatory T helper cells, termed Th17 cells, that are major contributors to autoimmune disease. We show here that the orphan nuclear receptor ROR gamma t is the key transcription factor that orchestrates the differentiation of this effector cell lineage. ROR gamma t induces transcription of the genes encoding IL-17 and the related cytokine IL-17F in naive CD4(+) T helper cells and is required for their expression in response to IL-6 and TGF-beta, the cytokines known to induce IL-17. Th17 cells are constitutively present throughout the intestinal lamina propria, express ROR gamma t, and are absent in mice deficient for ROR gamma t or IL-6. Mice with ROR gamma t-deficient T cells have attenuated autoimmune disease and lack tissue-infiltrating Th17 cells. Together, these studies suggest that ROR gamma t is a key regulator of immune homeostasis and highlight its potential as a therapeutic target in inflammatory diseases.
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