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TGFbeta and retinoic acid intersect in immune-regulation

Daniel Mucida1, Hilde Cheroutre

  • 1La Jolla Institute for Allergy and Immunology, La Jolla, California 92037, USA.

Cell Adhesion & Migration
|March 6, 2009
PubMed

Transforming growth factor (TGFbeta) prevents T(H)1 and T(H)2 differentiation and converts naïve CD4 cells into Foxp3-expressing T regulatory (Treg) cell.(1,2) In sharp contrast, in the presence of pro-inflammatory cytokines, including IL-6, TGFbeta not only inhibits Foxp3 expression but also promotes the differentiation of pro-inflammatory IL17-producing CD4 effector T (T(H)17) cells.(3-5) This reciprocal TGFbeta-dependent differentiation imposes a critical dilemma between pro- and anti-inflammatory immunity and suggests that a sensitive regulatory mechanism must exist to control TGFbeta-driven T(H)17 effector and Treg differentiation. A vitamin A metabolite, retinoic acid (RA), was recently identified as a key modulator of TGFbeta-driven- immune deviation capable of suppressing T(H)17 differentiation while promoting Foxp3(+)Treg generation.(6-10).

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