TGFβ and Retinoic Acid Intersect in Immune-Regulation
Volume 1, Issue 3
Downloads and Tools
Pages 142 - 144http://dx.doi.org/10.4161/cam.1.3.5062
Authors: Daniel Mucida and Hilde Cheroutre View affiliations
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.
Received: August 16, 2007; Accepted: September 20, 2007