Abstract
The physiological regulation of the expression of interleukin (IL)-9, a cytokine traditionally regarded as being T(H)2 associated, remains unclear. Here, we show that IL-9-expressing T cells generated in vitro in the presence of transforming growth factor-beta and IL-4 express high levels of mRNA for IL-17 receptor B (IL-17RB), the receptor for IL-25. Treatment of these cells with IL-25 enhances IL-9 expression in vitro. Moreover, transgenic and retroviral overexpression of IL-17RB in T cells results in IL-25-induced IL-9 production that is IL-4 independent. In vivo, the IL-25-IL-17RB pathway regulates IL-9 expression in allergic airway inflammation. Thus, IL-25 is a newly identified regulator of IL-9 expression.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Bronchial Hyperreactivity / genetics
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Bronchial Hyperreactivity / immunology*
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Bronchoalveolar Lavage Fluid / cytology
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Bronchoalveolar Lavage Fluid / immunology
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Cell Count
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Disease Models, Animal
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Gene Expression Regulation
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Interleukin-9 / biosynthesis*
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Interleukin-9 / genetics
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Interleukin-9 / immunology
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Interleukins / immunology
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Interleukins / metabolism*
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Mice
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Mice, Transgenic
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RNA, Messenger / biosynthesis
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RNA, Messenger / genetics
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Receptors, Interleukin-17 / genetics
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Receptors, Interleukin-17 / immunology
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Reverse Transcriptase Polymerase Chain Reaction
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Signal Transduction
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T-Lymphocytes / immunology*
Substances
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Interleukin-9
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Interleukins
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Mydgf protein, mouse
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RNA, Messenger
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Receptors, Interleukin-17