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Commentary & View
TGFβ and Retinoic Acid Intersect in Immune-Regulation
Daniel Mucida and Hilde Cheroutre
Volume 1, Issue 3July/August/September 2007
Pages 142 - 144
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Transforming growth factor (TGFβ) prevents TH1 and TH2 differentiation and converts naïve CD4 cells into Foxp3-expressing T regulatory (Treg) cell1, 2. In sharp contrast, in the presence of pro-inflammatory cytokines, including IL-6, TGFβ not only inhibits Foxp3 expression but also promotes the differentiation of pro-inflammatory IL17-producing CD4 effector T (TH17) cells3-5. This reciprocal TGFβ-dependent differentiation imposes a critical dilemma between pro- and anti-inflammatory immunity and suggests that a sensitive regulatory mechanism must exist to control TGFβ-driven TH17 effector and Treg differentiation. A vitamin A metabolite, retinoic acid (RA), was recently identified as a key modulator of TGFβ-driven immune deviation capable of suppressing TH17 differentiation while promoting Foxp3+Treg generation 6-10.
Authors
- Daniel Mucida
- La Jolla Institute for Allergy and Immunology (LIAI)
- Hilde Cheroutre
- La Jolla Institute for Allergy and Immunology (LIAI)
We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link:
Download PDF
If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.
