Abstract
Mice deficient in the adaptor Ndfip1 develop inflammation at sites of environmental antigen exposure. We show here that such mice had fewer inducible regulatory T cells (iT(reg) cells). In vitro, Ndfip1-deficient T cells expressed normal amounts of the transcription factor Foxp3 during the first 48 h of iT(reg) cell differentiation; however, this expression was not sustained. Abortive Foxp3 expression was caused by production of interleukin 4 (IL-4) by Ndfip1(-/-) cells. We found that Ndfip1 expression was transiently upregulated during iT(reg) cell differentiation in a manner dependent on transforming growth factor-β (TGF-β). Once expressed, Ndfip1 promoted degradation of the transcription factor JunB mediated by the E3 ubiquitin ligase Itch, thus preventing IL-4 production. On the basis of our data, we propose that TGF-β signaling induces Ndfip1 expression to silence IL-4 production, thus permitting iT(reg) cell differentiation.
Publication types
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Research Support, N.I.H., Extramural
MeSH terms
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Animals
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Carrier Proteins / genetics*
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Cell Differentiation* / drug effects
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Cells, Cultured
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Forkhead Transcription Factors / genetics
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Forkhead Transcription Factors / metabolism
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Gene Expression Regulation
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Intercellular Signaling Peptides and Proteins
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Interleukin-4 / biosynthesis*
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Interleukin-4 / genetics
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Interleukin-4 / pharmacology
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Membrane Proteins / deficiency
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Membrane Proteins / genetics*
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Mice
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Mice, Inbred C57BL
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Mice, Knockout
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Proto-Oncogene Proteins c-jun / metabolism
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Signal Transduction
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T-Lymphocytes, Regulatory / cytology
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T-Lymphocytes, Regulatory / immunology*
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Transforming Growth Factor beta / pharmacology*
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Ubiquitin-Protein Ligases / deficiency
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Ubiquitin-Protein Ligases / genetics
Substances
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Carrier Proteins
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Forkhead Transcription Factors
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Foxp3 protein, mouse
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Intercellular Signaling Peptides and Proteins
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Membrane Proteins
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Ndfip1 protein, mouse
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Proto-Oncogene Proteins c-jun
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Transforming Growth Factor beta
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Interleukin-4
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Itch protein, mouse
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Ubiquitin-Protein Ligases